Human adipose-derived mesenchymal stem cells prevent type 1 diabetes induced by immune checkpoint blockade

Aims/hypothesis Immunomodulators blocking cytotoxic T-lymphocyte-associated protein 4 (CTLA-4) and programmed cell death protein 1 (PD-1) or programmed death-ligand 1 (PD-L1) have improved the treatment of a broad spectrum of cancers. These immune checkpoint inhibitors (ICIs) reactivate the immune s...

Full description

Saved in:
Bibliographic Details
Published inDiabetologia Vol. 65; no. 7; pp. 1185 - 1197
Main Authors Kawada-Horitani, Emi, Kita, Shunbun, Okita, Tomonori, Nakamura, Yuto, Nishida, Hiroyuki, Honma, Yoichi, Fukuda, Shiro, Tsugawa-Shimizu, Yuri, Kozawa, Junji, Sakaue, Takaaki, Kawachi, Yusuke, Fujishima, Yuya, Nishizawa, Hitoshi, Azuma, Miyuki, Maeda, Norikazu, Shimomura, Iichiro
Format Journal Article
LanguageEnglish
Published Berlin/Heidelberg Springer Berlin Heidelberg 01.07.2022
Springer Nature B.V
Subjects
Animals
Antibodies, Monoclonal
Apoptosis
B7-H1 Antigen - metabolism
Beta cells
Cancer
Cancer therapies
CD3 antigen
Cell death
Chemokines
CTLA-4 protein
Cytokines
Cytotoxicity
Diabetes
Diabetes mellitus (insulin dependent)
Diabetes Mellitus, Type 1 - metabolism
Fibrosis
Human Physiology
Humans
Immune Checkpoint Inhibitors
Immune system
Immunofluorescence
Immunomodulation
Insulin
Internal Medicine
Ligands
Lymphocytes
Lymphocytes T
Macrophages
Male
Medicine
Medicine & Public Health
Mesenchymal stem cells
Mesenchymal Stem Cells - metabolism
Metabolic Diseases
Metastases
Mice
Mice, Inbred NOD
Monoclonal antibodies
Monocytes
Neoplasms - metabolism
Patients
PD-1 protein
PD-L1 protein
Plasma
Programmed Cell Death 1 Receptor - metabolism
Stem cells
Tumors
Immune checkpoint inhibitor
NOD mouse
Mesenchymal stem cells
Online AccessGet full text

Cover

Abstract Aims/hypothesis Immunomodulators blocking cytotoxic T-lymphocyte-associated protein 4 (CTLA-4) and programmed cell death protein 1 (PD-1) or programmed death-ligand 1 (PD-L1) have improved the treatment of a broad spectrum of cancers. These immune checkpoint inhibitors (ICIs) reactivate the immune system against tumour cells but can also trigger autoimmune side effects, including type 1 diabetes. Mesenchymal stem cell (MSC) therapy is the most prevalent cell therapy, with tissue-regenerating, anti-fibrosis and immunomodulatory functions provided by the secretome of the cells. Here, we examined whether systemic MSC treatment could prevent the development of type 1 diabetes in a NOD mouse model. Methods The purified PD-L1 monoclonal antibody was administered to induce diabetes in male NOD mice which normally do not develop diabetes. Human adipose-derived MSCs were administered by tail vein injections. T cells, macrophages and monocyte-derived macrophages expressing C-X-C motif chemokine ligand 9 (CXCL9) in pancreatic sections of NOD mice and a cancer patient who developed diabetes following the ICI treatments were analysed by immunofluorescence. Tissue localisation of the injected MSCs, plasma exosome levels and plasma cytokine profiles were also investigated. Results PD-1/PD-L1 blockade induced diabetes in 16 of 25 (64%) NOD mice which received anti-PD-L1 mAb without hMSCs [MSC(−)], whereas MSC administration decreased the incidence to four of 21 (19%) NOD mice which received anti-PD-L1 mAb and hMSCs [MSC(+)]. The PD-1/PD-L1 blockade significantly increased the area of CD3-positive T cells (6.2-fold) and macrophage-2 (Mac-2) antigen (2.5-fold)- and CXCL9 (40.3-fold)-positive macrophages in the islets. MSCs significantly reduced T cell (45%) and CXCL9-positive macrophage (67%) accumulation in the islets and the occurrence of diabetes. The insulin content (1.9-fold) and islet beta cell area (2.7-fold) were also improved by MSCs. T cells and CXCL9-positive macrophages infiltrated into the intricate gaps between the beta cells in the islets by PD-1/PD-L1 blockade. Such immune cell infiltration was largely prevented by MSCs. The most striking difference was observed in the CXCL9-positive macrophages, which normally did not reside in the beta cell region in the islets but abundantly accumulated in this area after PD-1/PD-L1 blockade and were prevented by MSCs. The CXCL9-positive macrophages were also observed in the islets of a cancer patient who developed diabetes following the administration of ICIs but few CXCL9-positive macrophages were observed in a control patient. Mechanistically, the injected MSCs accumulated in the lung but not in the pancreas and strongly increased plasma exosome levels and changed plasma cytokine profiles. Conclusions/interpretation Our results suggest that MSCs can prevent the incidence of diabetes associated with immune checkpoint cancer therapy and may be worth further consideration for new adjuvant cell therapy. Graphical abstract
AbstractList Aims/hypothesisImmunomodulators blocking cytotoxic T-lymphocyte-associated protein 4 (CTLA-4) and programmed cell death protein 1 (PD-1) or programmed death-ligand 1 (PD-L1) have improved the treatment of a broad spectrum of cancers. These immune checkpoint inhibitors (ICIs) reactivate the immune system against tumour cells but can also trigger autoimmune side effects, including type 1 diabetes. Mesenchymal stem cell (MSC) therapy is the most prevalent cell therapy, with tissue-regenerating, anti-fibrosis and immunomodulatory functions provided by the secretome of the cells. Here, we examined whether systemic MSC treatment could prevent the development of type 1 diabetes in a NOD mouse model.MethodsThe purified PD-L1 monoclonal antibody was administered to induce diabetes in male NOD mice which normally do not develop diabetes. Human adipose-derived MSCs were administered by tail vein injections. T cells, macrophages and monocyte-derived macrophages expressing C-X-C motif chemokine ligand 9 (CXCL9) in pancreatic sections of NOD mice and a cancer patient who developed diabetes following the ICI treatments were analysed by immunofluorescence. Tissue localisation of the injected MSCs, plasma exosome levels and plasma cytokine profiles were also investigated.ResultsPD-1/PD-L1 blockade induced diabetes in 16 of 25 (64%) NOD mice which received anti-PD-L1 mAb without hMSCs [MSC(−)], whereas MSC administration decreased the incidence to four of 21 (19%) NOD mice which received anti-PD-L1 mAb and hMSCs [MSC(+)]. The PD-1/PD-L1 blockade significantly increased the area of CD3-positive T cells (6.2-fold) and macrophage-2 (Mac-2) antigen (2.5-fold)- and CXCL9 (40.3-fold)-positive macrophages in the islets. MSCs significantly reduced T cell (45%) and CXCL9-positive macrophage (67%) accumulation in the islets and the occurrence of diabetes. The insulin content (1.9-fold) and islet beta cell area (2.7-fold) were also improved by MSCs. T cells and CXCL9-positive macrophages infiltrated into the intricate gaps between the beta cells in the islets by PD-1/PD-L1 blockade. Such immune cell infiltration was largely prevented by MSCs. The most striking difference was observed in the CXCL9-positive macrophages, which normally did not reside in the beta cell region in the islets but abundantly accumulated in this area after PD-1/PD-L1 blockade and were prevented by MSCs. The CXCL9-positive macrophages were also observed in the islets of a cancer patient who developed diabetes following the administration of ICIs but few CXCL9-positive macrophages were observed in a control patient. Mechanistically, the injected MSCs accumulated in the lung but not in the pancreas and strongly increased plasma exosome levels and changed plasma cytokine profiles.Conclusions/interpretationOur results suggest that MSCs can prevent the incidence of diabetes associated with immune checkpoint cancer therapy and may be worth further consideration for new adjuvant cell therapy.
AIMS/HYPOTHESISImmunomodulators blocking cytotoxic T-lymphocyte-associated protein 4 (CTLA-4) and programmed cell death protein 1 (PD-1) or programmed death-ligand 1 (PD-L1) have improved the treatment of a broad spectrum of cancers. These immune checkpoint inhibitors (ICIs) reactivate the immune system against tumour cells but can also trigger autoimmune side effects, including type 1 diabetes. Mesenchymal stem cell (MSC) therapy is the most prevalent cell therapy, with tissue-regenerating, anti-fibrosis and immunomodulatory functions provided by the secretome of the cells. Here, we examined whether systemic MSC treatment could prevent the development of type 1 diabetes in a NOD mouse model. METHODSThe purified PD-L1 monoclonal antibody was administered to induce diabetes in male NOD mice which normally do not develop diabetes. Human adipose-derived MSCs were administered by tail vein injections. T cells, macrophages and monocyte-derived macrophages expressing C-X-C motif chemokine ligand 9 (CXCL9) in pancreatic sections of NOD mice and a cancer patient who developed diabetes following the ICI treatments were analysed by immunofluorescence. Tissue localisation of the injected MSCs, plasma exosome levels and plasma cytokine profiles were also investigated. RESULTSPD-1/PD-L1 blockade induced diabetes in 16 of 25 (64%) NOD mice which received anti-PD-L1 mAb without hMSCs [MSC(-)], whereas MSC administration decreased the incidence to four of 21 (19%) NOD mice which received anti-PD-L1 mAb and hMSCs [MSC(+)]. The PD-1/PD-L1 blockade significantly increased the area of CD3-positive T cells (6.2-fold) and macrophage-2 (Mac-2) antigen (2.5-fold)- and CXCL9 (40.3-fold)-positive macrophages in the islets. MSCs significantly reduced T cell (45%) and CXCL9-positive macrophage (67%) accumulation in the islets and the occurrence of diabetes. The insulin content (1.9-fold) and islet beta cell area (2.7-fold) were also improved by MSCs. T cells and CXCL9-positive macrophages infiltrated into the intricate gaps between the beta cells in the islets by PD-1/PD-L1 blockade. Such immune cell infiltration was largely prevented by MSCs. The most striking difference was observed in the CXCL9-positive macrophages, which normally did not reside in the beta cell region in the islets but abundantly accumulated in this area after PD-1/PD-L1 blockade and were prevented by MSCs. The CXCL9-positive macrophages were also observed in the islets of a cancer patient who developed diabetes following the administration of ICIs but few CXCL9-positive macrophages were observed in a control patient. Mechanistically, the injected MSCs accumulated in the lung but not in the pancreas and strongly increased plasma exosome levels and changed plasma cytokine profiles. CONCLUSIONS/INTERPRETATIONOur results suggest that MSCs can prevent the incidence of diabetes associated with immune checkpoint cancer therapy and may be worth further consideration for new adjuvant cell therapy.
Immunomodulators blocking cytotoxic T-lymphocyte-associated protein 4 (CTLA-4) and programmed cell death protein 1 (PD-1) or programmed death-ligand 1 (PD-L1) have improved the treatment of a broad spectrum of cancers. These immune checkpoint inhibitors (ICIs) reactivate the immune system against tumour cells but can also trigger autoimmune side effects, including type 1 diabetes. Mesenchymal stem cell (MSC) therapy is the most prevalent cell therapy, with tissue-regenerating, anti-fibrosis and immunomodulatory functions provided by the secretome of the cells. Here, we examined whether systemic MSC treatment could prevent the development of type 1 diabetes in a NOD mouse model. The purified PD-L1 monoclonal antibody was administered to induce diabetes in male NOD mice which normally do not develop diabetes. Human adipose-derived MSCs were administered by tail vein injections. T cells, macrophages and monocyte-derived macrophages expressing C-X-C motif chemokine ligand 9 (CXCL9) in pancreatic sections of NOD mice and a cancer patient who developed diabetes following the ICI treatments were analysed by immunofluorescence. Tissue localisation of the injected MSCs, plasma exosome levels and plasma cytokine profiles were also investigated. PD-1/PD-L1 blockade induced diabetes in 16 of 25 (64%) NOD mice which received anti-PD-L1 mAb without hMSCs [MSC(-)], whereas MSC administration decreased the incidence to four of 21 (19%) NOD mice which received anti-PD-L1 mAb and hMSCs [MSC(+)]. The PD-1/PD-L1 blockade significantly increased the area of CD3-positive T cells (6.2-fold) and macrophage-2 (Mac-2) antigen (2.5-fold)- and CXCL9 (40.3-fold)-positive macrophages in the islets. MSCs significantly reduced T cell (45%) and CXCL9-positive macrophage (67%) accumulation in the islets and the occurrence of diabetes. The insulin content (1.9-fold) and islet beta cell area (2.7-fold) were also improved by MSCs. T cells and CXCL9-positive macrophages infiltrated into the intricate gaps between the beta cells in the islets by PD-1/PD-L1 blockade. Such immune cell infiltration was largely prevented by MSCs. The most striking difference was observed in the CXCL9-positive macrophages, which normally did not reside in the beta cell region in the islets but abundantly accumulated in this area after PD-1/PD-L1 blockade and were prevented by MSCs. The CXCL9-positive macrophages were also observed in the islets of a cancer patient who developed diabetes following the administration of ICIs but few CXCL9-positive macrophages were observed in a control patient. Mechanistically, the injected MSCs accumulated in the lung but not in the pancreas and strongly increased plasma exosome levels and changed plasma cytokine profiles. Our results suggest that MSCs can prevent the incidence of diabetes associated with immune checkpoint cancer therapy and may be worth further consideration for new adjuvant cell therapy.
Aims/hypothesis Immunomodulators blocking cytotoxic T-lymphocyte-associated protein 4 (CTLA-4) and programmed cell death protein 1 (PD-1) or programmed death-ligand 1 (PD-L1) have improved the treatment of a broad spectrum of cancers. These immune checkpoint inhibitors (ICIs) reactivate the immune system against tumour cells but can also trigger autoimmune side effects, including type 1 diabetes. Mesenchymal stem cell (MSC) therapy is the most prevalent cell therapy, with tissue-regenerating, anti-fibrosis and immunomodulatory functions provided by the secretome of the cells. Here, we examined whether systemic MSC treatment could prevent the development of type 1 diabetes in a NOD mouse model. Methods The purified PD-L1 monoclonal antibody was administered to induce diabetes in male NOD mice which normally do not develop diabetes. Human adipose-derived MSCs were administered by tail vein injections. T cells, macrophages and monocyte-derived macrophages expressing C-X-C motif chemokine ligand 9 (CXCL9) in pancreatic sections of NOD mice and a cancer patient who developed diabetes following the ICI treatments were analysed by immunofluorescence. Tissue localisation of the injected MSCs, plasma exosome levels and plasma cytokine profiles were also investigated. Results PD-1/PD-L1 blockade induced diabetes in 16 of 25 (64%) NOD mice which received anti-PD-L1 mAb without hMSCs [MSC(−)], whereas MSC administration decreased the incidence to four of 21 (19%) NOD mice which received anti-PD-L1 mAb and hMSCs [MSC(+)]. The PD-1/PD-L1 blockade significantly increased the area of CD3-positive T cells (6.2-fold) and macrophage-2 (Mac-2) antigen (2.5-fold)- and CXCL9 (40.3-fold)-positive macrophages in the islets. MSCs significantly reduced T cell (45%) and CXCL9-positive macrophage (67%) accumulation in the islets and the occurrence of diabetes. The insulin content (1.9-fold) and islet beta cell area (2.7-fold) were also improved by MSCs. T cells and CXCL9-positive macrophages infiltrated into the intricate gaps between the beta cells in the islets by PD-1/PD-L1 blockade. Such immune cell infiltration was largely prevented by MSCs. The most striking difference was observed in the CXCL9-positive macrophages, which normally did not reside in the beta cell region in the islets but abundantly accumulated in this area after PD-1/PD-L1 blockade and were prevented by MSCs. The CXCL9-positive macrophages were also observed in the islets of a cancer patient who developed diabetes following the administration of ICIs but few CXCL9-positive macrophages were observed in a control patient. Mechanistically, the injected MSCs accumulated in the lung but not in the pancreas and strongly increased plasma exosome levels and changed plasma cytokine profiles. Conclusions/interpretation Our results suggest that MSCs can prevent the incidence of diabetes associated with immune checkpoint cancer therapy and may be worth further consideration for new adjuvant cell therapy. Graphical abstract
Author Honma, Yoichi
Okita, Tomonori
Kozawa, Junji
Tsugawa-Shimizu, Yuri
Nishizawa, Hitoshi
Fujishima, Yuya
Maeda, Norikazu
Fukuda, Shiro
Kita, Shunbun
Kawachi, Yusuke
Kawada-Horitani, Emi
Nishida, Hiroyuki
Nakamura, Yuto
Azuma, Miyuki
Sakaue, Takaaki
Shimomura, Iichiro
Author_xml – sequence: 1
  givenname: Emi
  orcidid: 0000-0003-1434-9214
  surname: Kawada-Horitani
  fullname: Kawada-Horitani, Emi
  organization: Department of Metabolic Medicine, Graduate School of Medicine, Osaka University
– sequence: 2
  givenname: Shunbun
  orcidid: 0000-0002-8937-0053
  surname: Kita
  fullname: Kita, Shunbun
  email: shunkita@endmet.med.osaka-u.ac.jp
  organization: Department of Metabolic Medicine, Graduate School of Medicine, Osaka University, Department of Adipose Management, Graduate School of Medicine, Osaka University
– sequence: 3
  givenname: Tomonori
  surname: Okita
  fullname: Okita, Tomonori
  organization: Department of Metabolic Medicine, Graduate School of Medicine, Osaka University
– sequence: 4
  givenname: Yuto
  surname: Nakamura
  fullname: Nakamura, Yuto
  organization: Department of Metabolic Medicine, Graduate School of Medicine, Osaka University
– sequence: 5
  givenname: Hiroyuki
  surname: Nishida
  fullname: Nishida, Hiroyuki
  organization: ROHTO Pharmaceutical Co., Ltd
– sequence: 6
  givenname: Yoichi
  surname: Honma
  fullname: Honma, Yoichi
  organization: ROHTO Pharmaceutical Co., Ltd
– sequence: 7
  givenname: Shiro
  surname: Fukuda
  fullname: Fukuda, Shiro
  organization: Department of Metabolic Medicine, Graduate School of Medicine, Osaka University
– sequence: 8
  givenname: Yuri
  surname: Tsugawa-Shimizu
  fullname: Tsugawa-Shimizu, Yuri
  organization: Department of Metabolic Medicine, Graduate School of Medicine, Osaka University
– sequence: 9
  givenname: Junji
  surname: Kozawa
  fullname: Kozawa, Junji
  organization: Department of Metabolic Medicine, Graduate School of Medicine, Osaka University, Department of Diabetes Care Medicine, Graduate School of Medicine, Osaka University
– sequence: 10
  givenname: Takaaki
  surname: Sakaue
  fullname: Sakaue, Takaaki
  organization: Department of Metabolic Medicine, Graduate School of Medicine, Osaka University
– sequence: 11
  givenname: Yusuke
  surname: Kawachi
  fullname: Kawachi, Yusuke
  organization: Department of Metabolic Medicine, Graduate School of Medicine, Osaka University
– sequence: 12
  givenname: Yuya
  surname: Fujishima
  fullname: Fujishima, Yuya
  organization: Department of Metabolic Medicine, Graduate School of Medicine, Osaka University
– sequence: 13
  givenname: Hitoshi
  surname: Nishizawa
  fullname: Nishizawa, Hitoshi
  organization: Department of Metabolic Medicine, Graduate School of Medicine, Osaka University
– sequence: 14
  givenname: Miyuki
  surname: Azuma
  fullname: Azuma, Miyuki
  organization: Department of Molecular Immunology, Graduate School of Medical and Dental Sciences, Tokyo Medical and Dental University
– sequence: 15
  givenname: Norikazu
  surname: Maeda
  fullname: Maeda, Norikazu
  organization: Department of Metabolic Medicine, Graduate School of Medicine, Osaka University, Department of Metabolism and Atherosclerosis, Graduate School of Medicine, Osaka University
– sequence: 16
  givenname: Iichiro
  surname: Shimomura
  fullname: Shimomura, Iichiro
  organization: Department of Metabolic Medicine, Graduate School of Medicine, Osaka University
BackLink https://www.ncbi.nlm.nih.gov/pubmed/35511238$$D View this record in MEDLINE/PubMed
BookMark eNp9kU9v1DAQxS1URLeFL8ABWeLCJTCO49i5IKEKKFIlLiBxsxx70vU2sYOdrLTfHi9byp8DJ2v0fvM8M--CnIUYkJDnDF4zAPkmA7BaVFDXFQgJquKPyIY1vJRNrc7I5qhXTLXfzslFzjsA4KJpn5BzLgRjNVcbsrteJxOocX6OGSuHye_R0QkzBrs9TGakecGJWhzHTOeEewwLXQ4zUkadNz0umKkPbrWlrT9QP01rQGq3aO_m6Avcj9HeGYdPyePBjBmf3b-X5OuH91-urqubzx8_Xb27qazoxFJ1TDABfdM00BnZW2hx6JS11kjTDu6o9EqwZrBoeN9aNdgWnMJCG66c5Zfk7cl3XvsJnS0DJzPqOfnJpIOOxuu_leC3-jbudcdkOZ4qBq_uDVL8vmJe9OTz8QAmYFyzrtsWoOuUrAv68h90F9cUynqFklwykAoKVZ8om2LOCYeHYRjoY5T6FKUuUeqfUWpeml78ucZDy6_sCsBPQC5SuMX0--__2P4AcrCt_g
CitedBy_id crossref_primary_10_3389_fmats_2023_1152378
crossref_primary_10_3390_vaccines10101691
crossref_primary_10_23736_S2724_542X_23_02944_9
crossref_primary_10_1016_j_intimp_2023_110414
crossref_primary_10_7759_cureus_60565
crossref_primary_10_7759_cureus_27337
crossref_primary_10_1007_s12015_022_10474_1
crossref_primary_10_1016_j_cej_2024_150561
crossref_primary_10_1089_scd_2024_0017
crossref_primary_10_3389_fcell_2022_956274
crossref_primary_10_3390_biom14040483
crossref_primary_10_3389_fnins_2024_1269577
crossref_primary_10_1186_s12974_024_03114_7
crossref_primary_10_1155_2023_9517826
crossref_primary_10_3390_ijms25115974
crossref_primary_10_1007_s12020_024_03942_w
crossref_primary_10_3389_fendo_2023_1157805
crossref_primary_10_2147_IJN_S451642
crossref_primary_10_1038_s41598_024_51935_6
crossref_primary_10_14348_molcells_2022_0110
crossref_primary_10_2337_db22_0557
crossref_primary_10_54097_hset_v54i_9758
crossref_primary_10_2147_IJN_S422416
Cites_doi 10.2337/dbi18-0002
10.1002/eji.200324084
10.1016/S2213-8587(19)30072-5
10.3389/fbioe.2020.00043
10.1210/jc.2016-2300
10.2337/db14-0656
10.1016/j.ejca.2020.09.033
10.1007/s13340-018-0362-2
10.1038/s41581-018-0023-5
10.1001/jamanetworkopen.2020.0423
10.1084/jem.20051776
10.1038/s41467-020-17670-y
10.3389/fimmu.2019.01191
10.2337/diacare.26.3.832
10.1038/s41598-018-25700-5
10.1073/pnas.2019743117
10.1210/jc.2019-00423
10.1158/1078-0432.CCR-19-1868
10.1038/ncpendmet0351
10.1073/pnas.0505497102
10.1136/jitc-2020-001361
10.1038/s41598-018-26471-9
10.4049/jimmunol.181.7.4832
10.1161/CIRCRESAHA.109.210682
10.1007/s00125-009-1374-z
10.2337/dc18-2518
10.1530/ERC-17-0358
10.1084/jem.20022125
10.1093/jb/mvaa105
10.1073/pnas.1718217115
10.1186/s13287-018-1053-4
10.1016/j.ymthe.2020.06.026
10.3727/096368913X665576
10.1136/bmjdrc-2018-000591
10.1136/jitc-2020-002045
10.1093/intimm/8.5.765
10.3402/jev.v4.26238
10.1001/jamaoncol.2017.3064
ContentType Journal Article
Copyright The Author(s) 2022
2022. The Author(s).
The Author(s) 2022. This work is published under http://creativecommons.org/licenses/by/4.0/. (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.
Copyright_xml – notice: The Author(s) 2022
– notice: 2022. The Author(s).
– notice: The Author(s) 2022. This work is published under http://creativecommons.org/licenses/by/4.0/. (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.
DBID C6C
CGR
CUY
CVF
ECM
EIF
NPM
AAYXX
CITATION
3V.
7T5
7X7
7XB
88E
8AO
8C1
8FI
8FJ
8FK
ABUWG
AFKRA
BENPR
CCPQU
FYUFA
GHDGH
H94
K9.
M0S
M1P
PQEST
PQQKQ
PQUKI
PRINS
7X8
5PM
DOI 10.1007/s00125-022-05708-3
DatabaseName SpringerOpen (Open Access)
Medline
MEDLINE
MEDLINE (Ovid)
MEDLINE
MEDLINE
PubMed
CrossRef
ProQuest Central (Corporate)
Immunology Abstracts
ProQuest Health & Medical Collection
ProQuest Central (purchase pre-March 2016)
Medical Database (Alumni Edition)
ProQuest Pharma Collection
Public Health Database (Proquest)
Hospital Premium Collection
Hospital Premium Collection (Alumni Edition)
ProQuest Central (Alumni) (purchase pre-March 2016)
ProQuest Central (Alumni)
ProQuest Central
ProQuest Central
ProQuest One Community College
Health Research Premium Collection
Health Research Premium Collection (Alumni)
AIDS and Cancer Research Abstracts
ProQuest Health & Medical Complete (Alumni)
Health & Medical Collection (Alumni Edition)
PML(ProQuest Medical Library)
ProQuest One Academic Eastern Edition (DO NOT USE)
ProQuest One Academic
ProQuest One Academic UKI Edition
ProQuest Central China
MEDLINE - Academic
PubMed Central (Full Participant titles)
DatabaseTitle MEDLINE
Medline Complete
MEDLINE with Full Text
PubMed
MEDLINE (Ovid)
CrossRef
ProQuest Public Health
ProQuest One Academic Eastern Edition
ProQuest Health & Medical Complete (Alumni)
ProQuest Central (Alumni Edition)
ProQuest One Community College
ProQuest Hospital Collection
Health Research Premium Collection (Alumni)
ProQuest Pharma Collection
ProQuest Central China
ProQuest Hospital Collection (Alumni)
ProQuest Central
ProQuest Health & Medical Complete
Health Research Premium Collection
ProQuest Medical Library
ProQuest One Academic UKI Edition
Health and Medicine Complete (Alumni Edition)
AIDS and Cancer Research Abstracts
Immunology Abstracts
ProQuest One Academic
ProQuest Medical Library (Alumni)
ProQuest Central (Alumni)
MEDLINE - Academic
DatabaseTitleList ProQuest Public Health
MEDLINE - Academic
MEDLINE
Database_xml – sequence: 1
  dbid: C6C
  name: SpringerOpen (Open Access)
  url: http://www.springeropen.com/
  sourceTypes: Publisher
– sequence: 2
  dbid: NPM
  name: PubMed
  url: https://proxy.k.utb.cz/login?url=http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed
  sourceTypes: Index Database
– sequence: 3
  dbid: EIF
  name: MEDLINE
  url: https://proxy.k.utb.cz/login?url=https://www.webofscience.com/wos/medline/basic-search
  sourceTypes: Index Database
– sequence: 4
  dbid: 7X7
  name: ProQuest Health & Medical Collection
  url: https://search.proquest.com/healthcomplete
  sourceTypes: Aggregation Database
DeliveryMethod fulltext_linktorsrc
Discipline Medicine
EISSN 1432-0428
EndPage 1197
ExternalDocumentID 10_1007_s00125_022_05708_3
35511238
Genre Journal Article
GrantInformation_xml – fundername: Japan Agency for Medical Research and Development
  grantid: A-85B
  funderid: http://dx.doi.org/10.13039/100009619
– fundername: Japan Science and Technology Agency
  grantid: 20233913
  funderid: http://dx.doi.org/10.13039/501100002241
– fundername: Japan Science and Technology Agency
  grantid: 20233913
– fundername: Japan Agency for Medical Research and Development
  grantid: A-85B
– fundername: ;
  grantid: A-85B
– fundername: ;
  grantid: 20233913
GroupedDBID ---
-53
-5E
-5G
-BR
-EM
-Y2
-~C
.55
.86
.GJ
.VR
06C
06D
0R~
0VY
199
1CY
1N0
1SB
2.D
203
28-
29F
29G
29~
2J2
2JN
2JY
2KG
2KM
2LR
2P1
2VQ
2~H
30V
36B
3O-
3V.
4.4
406
408
409
40D
40E
53G
5GY
5QI
5RE
5VS
67Z
6NX
78A
7X7
88E
8AO
8C1
8FI
8FJ
8TC
8UJ
95-
95.
95~
96X
A8Z
AAAVM
AABHQ
AABYN
AAFGU
AAHNG
AAIAL
AAJKR
AAKSU
AANXM
AANZL
AAPBV
AARHV
AARTL
AATNV
AATVU
AAUYE
AAWCG
AAYFA
AAYIU
AAYQN
AAYTO
ABBBX
ABBXA
ABDZT
ABECU
ABFGW
ABFTV
ABHLI
ABHQN
ABIPD
ABJNI
ABJOX
ABKAS
ABKCH
ABKTR
ABLJU
ABMNI
ABMQK
ABNWP
ABOCM
ABPLI
ABQBU
ABSXP
ABTEG
ABTKH
ABTMW
ABULA
ABUWG
ABUWZ
ABWNU
ABXPI
ACBMV
ACBRV
ACBXY
ACBYP
ACGFS
ACHSB
ACHXU
ACIGE
ACIPQ
ACKNC
ACMDZ
ACMLO
ACOKC
ACOMO
ACPRK
ACTTH
ACUDM
ACVWB
ACWMK
ADBBV
ADHHG
ADHIR
ADIMF
ADINQ
ADJJI
ADKNI
ADKPE
ADMDM
ADOXG
ADRFC
ADTPH
ADURQ
ADYFF
ADZKW
AEBTG
AEEQQ
AEFIE
AEFTE
AEGAL
AEGNC
AEJHL
AEJRE
AEKMD
AENEX
AEOHA
AEPYU
AEQTP
AESKC
AESTI
AETLH
AEVLU
AEVTX
AEXYK
AFAFS
AFDYV
AFEXP
AFFNX
AFJLC
AFKRA
AFLOW
AFNRJ
AFQWF
AFWTZ
AFZKB
AGAYW
AGDGC
AGGBP
AGJBK
AGKHE
AGMZJ
AGQMX
AGWIL
AGWZB
AGYKE
AHAVH
AHBYD
AHIZS
AHKAY
AHMBA
AHSBF
AHVUH
AHYZX
AIAKS
AIIXL
AILAN
AIMYW
AITGF
AJBLW
AJDOV
AJRNO
AJZVZ
AKMHD
AKQUC
ALMA_UNASSIGNED_HOLDINGS
ALWAN
AMKLP
AMXSW
AMYLF
AMYQR
AOCGG
ARMRJ
ASPBG
AVWKF
AXYYD
AZFZN
B-.
BA0
BBWZM
BDATZ
BENPR
BGNMA
BPHCQ
BVXVI
C6C
CAG
CCPQU
COF
CS3
CSCUP
DDRTE
DL5
DNIVK
DPUIP
EBLON
EBS
EIOEI
EJD
EMB
EMOBN
EN4
ESBYG
ESTFP
F5P
FEDTE
FERAY
FFXSO
FIGPU
FINBP
FNLPD
FRRFC
FSGXE
FWDCC
FYUFA
G-Y
G-Z
GGCAI
GGRSB
GJIRD
GNWQR
GQ6
GQ7
GQ8
GRRUI
GXS
HF~
HG5
HG6
HMCUK
HMJXF
HQYDN
HRMNR
HVGLF
HZ~
I09
IHE
IJ-
IKXTQ
IMOTQ
ITM
IWAJR
IXC
IZIGR
IZQ
I~X
I~Z
J-C
J0Z
J5H
JBSCW
JCJTX
JZLTJ
KDC
KOV
KOW
KPH
L7B
LAS
LLZTM
M1P
M4Y
MA-
MVM
N2Q
N9A
NB0
NDZJH
NPVJJ
NQJWS
NU0
O9-
O93
O9G
O9I
O9J
OAM
OVD
P19
P2P
P6G
P9S
PF0
PQQKQ
PROAC
PSQYO
PT4
Q2X
QOK
QOR
QOS
R4E
R89
R9I
RHV
RIG
ROL
RPX
RRX
RSV
S16
S1Z
S26
S27
S28
S37
S3B
SAP
SCLPG
SDE
SDH
SDM
SHX
SISQX
SJYHP
SMD
SNE
SNPRN
SNX
SOHCF
SOJ
SPISZ
SRMVM
SSLCW
SSXJD
STPWE
SV3
SZ9
SZN
T13
T16
TEORI
TR2
TSG
TSK
TSV
TT1
TUC
U2A
U9L
UG4
UKHRP
UNUBA
UOJIU
UTJUX
UZXMN
VC2
VFIZW
W23
W48
WH7
WJK
WK8
X7M
YLTOR
Z45
Z5O
Z7U
Z7V
Z7W
Z7X
Z7Z
Z81
Z82
Z83
Z86
Z87
Z88
Z8O
Z8P
Z8Q
Z8T
Z8U
Z8V
Z8W
Z91
Z92
ZA5
ZGI
ZMTXR
ZOVNA
~EX
~KM
AACDK
AAEOY
AAEWM
AAJBT
AASML
AAYZH
ABAKF
ACAOD
ACDTI
ACZOJ
AEFQL
AEMSY
AFBBN
AGQEE
AGRTI
AIGIU
AJOOF
ALIPV
CGR
CUY
CVF
ECM
EIF
H13
NPM
AAYXX
ABQSL
CITATION
7T5
7XB
8FK
H94
K9.
PQEST
PQUKI
PRINS
7X8
5PM
ID FETCH-LOGICAL-c595t-915150b44409a7bc06ef98ccca7a6fd0b44b8514fcea3b6c8fc60d8e09aa38dc3
IEDL.DBID U2A
ISSN 0012-186X
IngestDate Tue Sep 17 21:18:32 EDT 2024
Wed Dec 04 10:35:57 EST 2024
Thu Oct 10 15:06:16 EDT 2024
Fri Dec 06 01:25:22 EST 2024
Wed Oct 16 00:41:03 EDT 2024
Sat Dec 16 12:08:00 EST 2023
IsDoiOpenAccess true
IsOpenAccess true
IsPeerReviewed true
IsScholarly true
Issue 7
Keywords Immune checkpoint inhibitor
NOD mouse
Mesenchymal stem cells
Language English
License 2022. The Author(s).
This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/.
LinkModel DirectLink
MergedId FETCHMERGED-LOGICAL-c595t-915150b44409a7bc06ef98ccca7a6fd0b44b8514fcea3b6c8fc60d8e09aa38dc3
Notes ObjectType-Article-1
SourceType-Scholarly Journals-1
ObjectType-Feature-2
content type line 23
ORCID 0000-0003-1434-9214
0000-0002-8937-0053
OpenAccessLink http://link.springer.com/10.1007/s00125-022-05708-3
PMID 35511238
PQID 2673710780
PQPubID 48469
PageCount 13
ParticipantIDs pubmedcentral_primary_oai_pubmedcentral_nih_gov_9174328
proquest_miscellaneous_2660099872
proquest_journals_2673710780
crossref_primary_10_1007_s00125_022_05708_3
pubmed_primary_35511238
springer_journals_10_1007_s00125_022_05708_3
PublicationCentury 2000
PublicationDate 2022-07-01
PublicationDateYYYYMMDD 2022-07-01
PublicationDate_xml – month: 07
  year: 2022
  text: 2022-07-01
  day: 01
PublicationDecade 2020
PublicationPlace Berlin/Heidelberg
PublicationPlace_xml – name: Berlin/Heidelberg
– name: Germany
– name: Heidelberg
PublicationSubtitle Clinical, Translational and Experimental Diabetes and Metabolism
PublicationTitle Diabetologia
PublicationTitleAbbrev Diabetologia
PublicationTitleAlternate Diabetologia
PublicationYear 2022
Publisher Springer Berlin Heidelberg
Springer Nature B.V
Publisher_xml – name: Springer Berlin Heidelberg
– name: Springer Nature B.V
References Carlsson, Schwarcz, Korsgren, Le Blanc (CR21) 2015; 64
Kita, Shimomura (CR32) 2021; 169
Ahn, Araki, Hashimoto (CR11) 2018; 115
Shi, Wang, Li (CR18) 2018; 14
Perdigoto, Quandt, Anderson, Herold (CR33) 2019; 7
Osum, Burrack, Martinov (CR14) 2018; 8
Nakamura, Kita, Tanaka (CR20) 2020; 28
Tsushima, Iwai, Otsuki (CR25) 2003; 33
Hmadcha, Martin-Montalvo, Gauthier, Soria, Capilla-Gonzalez (CR36) 2020; 8
Keir, Liang, Guleria (CR15) 2006; 203
Oestreich, Yoon, Ahmed, Boss (CR12) 2008; 181
Stamatouli, Quandt, Perdigoto (CR4) 2018; 67
Madec, Mallone, Afonso (CR23) 2009; 52
Hu, Zakharov, Peterson, Unanue (CR26) 2020; 117
Cukier, Santini, Scaranti, Hoff (CR2) 2017; 24
Steffes, Sibley, Jackson, Thomas (CR10) 2003; 26
Weiss, Dahlke (CR27) 2019; 10
Yoneda, Imagawa, Hosokawa (CR24) 2019; 42
de Filette, Jansen, Schreuer (CR5) 2016; 101
Bhansali, Asokumar, Walia (CR22) 2014; 23
Ansari, Salama, Chitnis (CR16) 2003; 198
House, Savas, Lai (CR29) 2020; 26
Marcovecchio, Thomas, Salek-Ardakani (CR30) 2021; 9
Hanafusa, Imagawa (CR9) 2007; 3
CR3
Buti, Bersanelli, Perrone (CR35) 2021; 142
Haslam, Gill, Prasad (CR38) 2020; 3
Wang, Yoshida, Nakaki, Hiai, Okazaki, Honjo (CR17) 2005; 102
Imai, Takahashi, Nishikawa (CR31) 2015; 4
Baden, Imagawa, Abiru (CR8) 2019; 10
Robert (CR1) 2020; 11
Kotwal, Haddox, Block, Kudva (CR7) 2019; 7
Agata, Kawasaki, Nishimura (CR13) 1996; 8
Chimenti, Smith, Li (CR19) 2010; 106
Cortellini, Tucci, Adamo (CR34) 2020; 8
Tsang, McGrath, Clifton-Bligh (CR6) 2019; 104
Liang, Zhang, Kong (CR37) 2018; 9
Leuning, Beijer, du Fosse (CR28) 2018; 8
S Buti (5708_CR35) 2021; 142
P Cukier (5708_CR2) 2017; 24
MY Baden (5708_CR8) 2019; 10
A Kotwal (5708_CR7) 2019; 7
ARR Weiss (5708_CR27) 2019; 10
F Tsushima (5708_CR25) 2003; 33
J Wang (5708_CR17) 2005; 102
PO Carlsson (5708_CR21) 2015; 64
A Hmadcha (5708_CR36) 2020; 8
T Hanafusa (5708_CR9) 2007; 3
IG House (5708_CR29) 2020; 26
KC Osum (5708_CR14) 2018; 8
Y Nakamura (5708_CR20) 2020; 28
H Hu (5708_CR26) 2020; 117
KJ Oestreich (5708_CR12) 2008; 181
E Ahn (5708_CR11) 2018; 115
A Bhansali (5708_CR22) 2014; 23
Y Shi (5708_CR18) 2018; 14
I Chimenti (5708_CR19) 2010; 106
Y Agata (5708_CR13) 1996; 8
ME Keir (5708_CR15) 2006; 203
S Yoneda (5708_CR24) 2019; 42
A Cortellini (5708_CR34) 2020; 8
VHM Tsang (5708_CR6) 2019; 104
T Imai (5708_CR31) 2015; 4
AL Perdigoto (5708_CR33) 2019; 7
5708_CR3
AM Madec (5708_CR23) 2009; 52
A Haslam (5708_CR38) 2020; 3
C Robert (5708_CR1) 2020; 11
AM Stamatouli (5708_CR4) 2018; 67
MW Steffes (5708_CR10) 2003; 26
J de Filette (5708_CR5) 2016; 101
MJ Ansari (5708_CR16) 2003; 198
S Kita (5708_CR32) 2021; 169
PM Marcovecchio (5708_CR30) 2021; 9
J Liang (5708_CR37) 2018; 9
DG Leuning (5708_CR28) 2018; 8
References_xml – volume: 67
  start-page: 1471
  issue: 8
  year: 2018
  end-page: 1480
  ident: CR4
  article-title: Collateral Damage: Insulin-Dependent Diabetes Induced With Checkpoint Inhibitors
  publication-title: Diabetes
  doi: 10.2337/dbi18-0002
  contributor:
    fullname: Perdigoto
– volume: 33
  start-page: 2773
  issue: 10
  year: 2003
  end-page: 2782
  ident: CR25
  article-title: Preferential contribution of B7-H1 to programmed death-1-mediated regulation of hapten-specific allergic inflammatory responses
  publication-title: Eur J Immunol
  doi: 10.1002/eji.200324084
  contributor:
    fullname: Otsuki
– volume: 7
  start-page: 421
  issue: 6
  year: 2019
  end-page: 423
  ident: CR33
  article-title: Checkpoint inhibitor-induced insulin-dependent diabetes: an emerging syndrome
  publication-title: Lancet Diabetes Endocrinol
  doi: 10.1016/S2213-8587(19)30072-5
  contributor:
    fullname: Herold
– volume: 8
  start-page: 43
  year: 2020
  ident: CR36
  article-title: Therapeutic Potential of Mesenchymal Stem Cells for Cancer Therapy
  publication-title: Front Bioeng Biotechnol
  doi: 10.3389/fbioe.2020.00043
  contributor:
    fullname: Capilla-Gonzalez
– volume: 101
  start-page: 4431
  issue: 11
  year: 2016
  end-page: 4439
  ident: CR5
  article-title: Incidence of Thyroid-Related Adverse Events in Melanoma Patients Treated With Pembrolizumab
  publication-title: J Clin Endocrinol Metab
  doi: 10.1210/jc.2016-2300
  contributor:
    fullname: Schreuer
– volume: 64
  start-page: 587
  issue: 2
  year: 2015
  end-page: 592
  ident: CR21
  article-title: Preserved beta-cell function in type 1 diabetes by mesenchymal stromal cells
  publication-title: Diabetes
  doi: 10.2337/db14-0656
  contributor:
    fullname: Le Blanc
– volume: 142
  start-page: 18
  year: 2021
  end-page: 28
  ident: CR35
  article-title: Effect of concomitant medications with immune-modulatory properties on the outcomes of patients with advanced cancer treated with immune checkpoint inhibitors: development and validation of a novel prognostic index
  publication-title: Eur J Cancer
  doi: 10.1016/j.ejca.2020.09.033
  contributor:
    fullname: Perrone
– volume: 10
  start-page: 58
  issue: 1
  year: 2019
  end-page: 66
  ident: CR8
  article-title: Characteristics and clinical course of type 1 diabetes mellitus related to anti-programmed cell death-1 therapy
  publication-title: Diabetol Int
  doi: 10.1007/s13340-018-0362-2
  contributor:
    fullname: Abiru
– volume: 14
  start-page: 493
  issue: 8
  year: 2018
  end-page: 507
  ident: CR18
  article-title: Immunoregulatory mechanisms of mesenchymal stem and stromal cells in inflammatory diseases
  publication-title: Nat Rev Nephrol
  doi: 10.1038/s41581-018-0023-5
  contributor:
    fullname: Li
– volume: 3
  start-page: e200423
  issue: 3
  year: 2020
  ident: CR38
  article-title: Estimation of the Percentage of US Patients With Cancer Who Are Eligible for Immune Checkpoint Inhibitor Drugs
  publication-title: JAMA Netw Open
  doi: 10.1001/jamanetworkopen.2020.0423
  contributor:
    fullname: Prasad
– volume: 203
  start-page: 883
  issue: 4
  year: 2006
  end-page: 895
  ident: CR15
  article-title: Tissue expression of PD-L1 mediates peripheral T cell tolerance
  publication-title: J Exp Med
  doi: 10.1084/jem.20051776
  contributor:
    fullname: Guleria
– volume: 11
  start-page: 3801
  issue: 1
  year: 2020
  ident: CR1
  article-title: A decade of immune-checkpoint inhibitors in cancer therapy
  publication-title: Nat Commun
  doi: 10.1038/s41467-020-17670-y
  contributor:
    fullname: Robert
– volume: 10
  start-page: 1191
  year: 2019
  ident: CR27
  article-title: Immunomodulation by Mesenchymal Stem Cells (MSCs): Mechanisms of Action of Living, Apoptotic, and Dead MSCs
  publication-title: Front Immunol
  doi: 10.3389/fimmu.2019.01191
  contributor:
    fullname: Dahlke
– volume: 26
  start-page: 832
  issue: 3
  year: 2003
  end-page: 836
  ident: CR10
  article-title: Beta-cell function and the development of diabetes-related complications in the diabetes control and complications trial
  publication-title: Diabetes Care
  doi: 10.2337/diacare.26.3.832
  contributor:
    fullname: Thomas
– volume: 8
  start-page: 7716
  issue: 1
  year: 2018
  ident: CR28
  article-title: The cytokine secretion profile of mesenchymal stromal cells is determined by surface structure of the microenvironment
  publication-title: Sci Rep
  doi: 10.1038/s41598-018-25700-5
  contributor:
    fullname: du Fosse
– volume: 117
  start-page: 31319
  issue: 49
  year: 2020
  end-page: 31330
  ident: CR26
  article-title: Cytocidal macrophages in symbiosis with CD4 and CD8 T cells cause acute diabetes following checkpoint blockade of PD-1 in NOD mice
  publication-title: Proc Natl Acad Sci U S A
  doi: 10.1073/pnas.2019743117
  contributor:
    fullname: Unanue
– volume: 104
  start-page: 5499
  issue: 11
  year: 2019
  end-page: 5506
  ident: CR6
  article-title: Checkpoint Inhibitor-Associated Autoimmune Diabetes Is Distinct From Type 1 Diabetes
  publication-title: J Clin Endocrinol Metab
  doi: 10.1210/jc.2019-00423
  contributor:
    fullname: Clifton-Bligh
– volume: 26
  start-page: 487
  issue: 2
  year: 2020
  end-page: 504
  ident: CR29
  article-title: Macrophage-Derived CXCL9 and CXCL10 Are Required for Antitumor Immune Responses Following Immune Checkpoint Blockade
  publication-title: Clin Cancer Res
  doi: 10.1158/1078-0432.CCR-19-1868
  contributor:
    fullname: Lai
– volume: 3
  start-page: 36
  issue: 1
  year: 2007
  end-page: 45
  ident: CR9
  article-title: Fulminant type 1 diabetes: a novel clinical entity requiring special attention by all medical practitioners
  publication-title: Nat Clin Pract Endocrinol Metab
  doi: 10.1038/ncpendmet0351
  contributor:
    fullname: Imagawa
– volume: 102
  start-page: 11823
  issue: 33
  year: 2005
  end-page: 11828
  ident: CR17
  article-title: Establishment of NOD-Pdcd1-/- mice as an efficient animal model of type I diabetes
  publication-title: Proc Natl Acad Sci U S A
  doi: 10.1073/pnas.0505497102
  contributor:
    fullname: Honjo
– volume: 8
  start-page: e001361
  issue: 2
  year: 2020
  ident: CR34
  article-title: Integrated analysis of concomitant medications and oncological outcomes from PD-1/PD-L1 checkpoint inhibitors in clinical practice
  publication-title: J Immunother Cancer
  doi: 10.1136/jitc-2020-001361
  contributor:
    fullname: Adamo
– volume: 8
  start-page: 1
  issue: 1
  year: 2018
  end-page: 12
  ident: CR14
  article-title: Interferon-gamma drives programmed death-ligand 1 expression on islet β cells to limit T cell function during autoimmune diabetes
  publication-title: Sci Rep
  doi: 10.1038/s41598-018-26471-9
  contributor:
    fullname: Martinov
– volume: 181
  start-page: 4832
  issue: 7
  year: 2008
  end-page: 4839
  ident: CR12
  article-title: NFATc1 regulates PD-1 expression upon T cell activation
  publication-title: J Immunol
  doi: 10.4049/jimmunol.181.7.4832
  contributor:
    fullname: Boss
– volume: 106
  start-page: 971
  issue: 5
  year: 2010
  end-page: 980
  ident: CR19
  article-title: Relative roles of direct regeneration versus paracrine effects of human cardiosphere-derived cells transplanted into infarcted mice
  publication-title: Circ Res
  doi: 10.1161/CIRCRESAHA.109.210682
  contributor:
    fullname: Li
– volume: 52
  start-page: 1391
  issue: 7
  year: 2009
  end-page: 1399
  ident: CR23
  article-title: Mesenchymal stem cells protect NOD mice from diabetes by inducing regulatory T cells
  publication-title: Diabetologia
  doi: 10.1007/s00125-009-1374-z
  contributor:
    fullname: Afonso
– volume: 42
  start-page: e116
  issue: 7
  year: 2019
  end-page: e118
  ident: CR24
  article-title: T-Lymphocyte Infiltration to Islets in the Pancreas of a Patient Who Developed Type 1 Diabetes After Administration of Immune Checkpoint Inhibitors
  publication-title: Diabetes Care
  doi: 10.2337/dc18-2518
  contributor:
    fullname: Hosokawa
– volume: 24
  start-page: T331
  issue: 12
  year: 2017
  end-page: T347
  ident: CR2
  article-title: Endocrine side effects of cancer immunotherapy
  publication-title: Endocr Relat Cancer
  doi: 10.1530/ERC-17-0358
  contributor:
    fullname: Hoff
– volume: 198
  start-page: 63
  issue: 1
  year: 2003
  end-page: 69
  ident: CR16
  article-title: The programmed death-1 (PD-1) pathway regulates autoimmune diabetes in nonobese diabetic (NOD) mice
  publication-title: J Exp Med
  doi: 10.1084/jem.20022125
  contributor:
    fullname: Chitnis
– volume: 169
  start-page: 173
  issue: 2
  year: 2021
  end-page: 179
  ident: CR32
  article-title: Stimulation of exosome biogenesis by adiponectin, a circulating factor secreted from adipocytes
  publication-title: J Biochem
  doi: 10.1093/jb/mvaa105
  contributor:
    fullname: Shimomura
– ident: CR3
– volume: 115
  start-page: 4749
  issue: 18
  year: 2018
  end-page: 4754
  ident: CR11
  article-title: Role of PD-1 during effector CD8 T cell differentiation
  publication-title: Proc Natl Acad Sci
  doi: 10.1073/pnas.1718217115
  contributor:
    fullname: Hashimoto
– volume: 9
  start-page: 312
  issue: 1
  year: 2018
  ident: CR37
  article-title: Safety analysis in patients with autoimmune disease receiving allogeneic mesenchymal stem cells infusion: a long-term retrospective study
  publication-title: Stem Cell Res Ther
  doi: 10.1186/s13287-018-1053-4
  contributor:
    fullname: Kong
– volume: 28
  start-page: 2203
  issue: 10
  year: 2020
  end-page: 2219
  ident: CR20
  article-title: Adiponectin Stimulates Exosome Release to Enhance Mesenchymal Stem-Cell-Driven Therapy of Heart Failure in Mice
  publication-title: Mol Ther
  doi: 10.1016/j.ymthe.2020.06.026
  contributor:
    fullname: Tanaka
– volume: 23
  start-page: 1075
  issue: 9
  year: 2014
  end-page: 1085
  ident: CR22
  article-title: Efficacy and safety of autologous bone marrow-derived stem cell transplantation in patients with type 2 diabetes mellitus: a randomized placebo-controlled study
  publication-title: Cell Transplant
  doi: 10.3727/096368913X665576
  contributor:
    fullname: Walia
– volume: 7
  start-page: e000591
  issue: 1
  year: 2019
  ident: CR7
  article-title: Immune checkpoint inhibitors: an emerging cause of insulin-dependent diabetes
  publication-title: BMJ Open Diabetes Res Care
  doi: 10.1136/bmjdrc-2018-000591
  contributor:
    fullname: Kudva
– volume: 9
  start-page: e002045
  issue: 2
  year: 2021
  ident: CR30
  article-title: CXCL9-expressing tumor-associated macrophages: new players in the fight against cancer
  publication-title: J Immunother Cancer
  doi: 10.1136/jitc-2020-002045
  contributor:
    fullname: Salek-Ardakani
– volume: 8
  start-page: 765
  issue: 5
  year: 1996
  end-page: 772
  ident: CR13
  article-title: Expression of the PD-1 antigen on the surface of stimulated mouse T and B lymphocytes
  publication-title: Int Immunol
  doi: 10.1093/intimm/8.5.765
  contributor:
    fullname: Nishimura
– volume: 4
  start-page: 26238
  issue: 1
  year: 2015
  ident: CR31
  article-title: Macrophage-dependent clearance of systemically administered B16BL6-derived exosomes from the blood circulation in mice
  publication-title: J Extracell Vesicles
  doi: 10.3402/jev.v4.26238
  contributor:
    fullname: Nishikawa
– volume: 24
  start-page: T331
  issue: 12
  year: 2017
  ident: 5708_CR2
  publication-title: Endocr Relat Cancer
  doi: 10.1530/ERC-17-0358
  contributor:
    fullname: P Cukier
– volume: 8
  start-page: 7716
  issue: 1
  year: 2018
  ident: 5708_CR28
  publication-title: Sci Rep
  doi: 10.1038/s41598-018-25700-5
  contributor:
    fullname: DG Leuning
– volume: 33
  start-page: 2773
  issue: 10
  year: 2003
  ident: 5708_CR25
  publication-title: Eur J Immunol
  doi: 10.1002/eji.200324084
  contributor:
    fullname: F Tsushima
– volume: 64
  start-page: 587
  issue: 2
  year: 2015
  ident: 5708_CR21
  publication-title: Diabetes
  doi: 10.2337/db14-0656
  contributor:
    fullname: PO Carlsson
– volume: 7
  start-page: 421
  issue: 6
  year: 2019
  ident: 5708_CR33
  publication-title: Lancet Diabetes Endocrinol
  doi: 10.1016/S2213-8587(19)30072-5
  contributor:
    fullname: AL Perdigoto
– volume: 7
  start-page: e000591
  issue: 1
  year: 2019
  ident: 5708_CR7
  publication-title: BMJ Open Diabetes Res Care
  doi: 10.1136/bmjdrc-2018-000591
  contributor:
    fullname: A Kotwal
– volume: 8
  start-page: 43
  year: 2020
  ident: 5708_CR36
  publication-title: Front Bioeng Biotechnol
  doi: 10.3389/fbioe.2020.00043
  contributor:
    fullname: A Hmadcha
– volume: 9
  start-page: e002045
  issue: 2
  year: 2021
  ident: 5708_CR30
  publication-title: J Immunother Cancer
  doi: 10.1136/jitc-2020-002045
  contributor:
    fullname: PM Marcovecchio
– volume: 8
  start-page: 1
  issue: 1
  year: 2018
  ident: 5708_CR14
  publication-title: Sci Rep
  doi: 10.1038/s41598-018-26471-9
  contributor:
    fullname: KC Osum
– volume: 14
  start-page: 493
  issue: 8
  year: 2018
  ident: 5708_CR18
  publication-title: Nat Rev Nephrol
  doi: 10.1038/s41581-018-0023-5
  contributor:
    fullname: Y Shi
– volume: 3
  start-page: 36
  issue: 1
  year: 2007
  ident: 5708_CR9
  publication-title: Nat Clin Pract Endocrinol Metab
  doi: 10.1038/ncpendmet0351
  contributor:
    fullname: T Hanafusa
– volume: 4
  start-page: 26238
  issue: 1
  year: 2015
  ident: 5708_CR31
  publication-title: J Extracell Vesicles
  doi: 10.3402/jev.v4.26238
  contributor:
    fullname: T Imai
– volume: 142
  start-page: 18
  year: 2021
  ident: 5708_CR35
  publication-title: Eur J Cancer
  doi: 10.1016/j.ejca.2020.09.033
  contributor:
    fullname: S Buti
– volume: 3
  start-page: e200423
  issue: 3
  year: 2020
  ident: 5708_CR38
  publication-title: JAMA Netw Open
  doi: 10.1001/jamanetworkopen.2020.0423
  contributor:
    fullname: A Haslam
– volume: 106
  start-page: 971
  issue: 5
  year: 2010
  ident: 5708_CR19
  publication-title: Circ Res
  doi: 10.1161/CIRCRESAHA.109.210682
  contributor:
    fullname: I Chimenti
– volume: 10
  start-page: 1191
  year: 2019
  ident: 5708_CR27
  publication-title: Front Immunol
  doi: 10.3389/fimmu.2019.01191
  contributor:
    fullname: ARR Weiss
– volume: 102
  start-page: 11823
  issue: 33
  year: 2005
  ident: 5708_CR17
  publication-title: Proc Natl Acad Sci U S A
  doi: 10.1073/pnas.0505497102
  contributor:
    fullname: J Wang
– volume: 11
  start-page: 3801
  issue: 1
  year: 2020
  ident: 5708_CR1
  publication-title: Nat Commun
  doi: 10.1038/s41467-020-17670-y
  contributor:
    fullname: C Robert
– volume: 9
  start-page: 312
  issue: 1
  year: 2018
  ident: 5708_CR37
  publication-title: Stem Cell Res Ther
  doi: 10.1186/s13287-018-1053-4
  contributor:
    fullname: J Liang
– volume: 28
  start-page: 2203
  issue: 10
  year: 2020
  ident: 5708_CR20
  publication-title: Mol Ther
  doi: 10.1016/j.ymthe.2020.06.026
  contributor:
    fullname: Y Nakamura
– volume: 115
  start-page: 4749
  issue: 18
  year: 2018
  ident: 5708_CR11
  publication-title: Proc Natl Acad Sci
  doi: 10.1073/pnas.1718217115
  contributor:
    fullname: E Ahn
– ident: 5708_CR3
  doi: 10.1001/jamaoncol.2017.3064
– volume: 181
  start-page: 4832
  issue: 7
  year: 2008
  ident: 5708_CR12
  publication-title: J Immunol
  doi: 10.4049/jimmunol.181.7.4832
  contributor:
    fullname: KJ Oestreich
– volume: 8
  start-page: 765
  issue: 5
  year: 1996
  ident: 5708_CR13
  publication-title: Int Immunol
  doi: 10.1093/intimm/8.5.765
  contributor:
    fullname: Y Agata
– volume: 198
  start-page: 63
  issue: 1
  year: 2003
  ident: 5708_CR16
  publication-title: J Exp Med
  doi: 10.1084/jem.20022125
  contributor:
    fullname: MJ Ansari
– volume: 101
  start-page: 4431
  issue: 11
  year: 2016
  ident: 5708_CR5
  publication-title: J Clin Endocrinol Metab
  doi: 10.1210/jc.2016-2300
  contributor:
    fullname: J de Filette
– volume: 203
  start-page: 883
  issue: 4
  year: 2006
  ident: 5708_CR15
  publication-title: J Exp Med
  doi: 10.1084/jem.20051776
  contributor:
    fullname: ME Keir
– volume: 117
  start-page: 31319
  issue: 49
  year: 2020
  ident: 5708_CR26
  publication-title: Proc Natl Acad Sci U S A
  doi: 10.1073/pnas.2019743117
  contributor:
    fullname: H Hu
– volume: 23
  start-page: 1075
  issue: 9
  year: 2014
  ident: 5708_CR22
  publication-title: Cell Transplant
  doi: 10.3727/096368913X665576
  contributor:
    fullname: A Bhansali
– volume: 26
  start-page: 487
  issue: 2
  year: 2020
  ident: 5708_CR29
  publication-title: Clin Cancer Res
  doi: 10.1158/1078-0432.CCR-19-1868
  contributor:
    fullname: IG House
– volume: 169
  start-page: 173
  issue: 2
  year: 2021
  ident: 5708_CR32
  publication-title: J Biochem
  doi: 10.1093/jb/mvaa105
  contributor:
    fullname: S Kita
– volume: 67
  start-page: 1471
  issue: 8
  year: 2018
  ident: 5708_CR4
  publication-title: Diabetes
  doi: 10.2337/dbi18-0002
  contributor:
    fullname: AM Stamatouli
– volume: 10
  start-page: 58
  issue: 1
  year: 2019
  ident: 5708_CR8
  publication-title: Diabetol Int
  doi: 10.1007/s13340-018-0362-2
  contributor:
    fullname: MY Baden
– volume: 26
  start-page: 832
  issue: 3
  year: 2003
  ident: 5708_CR10
  publication-title: Diabetes Care
  doi: 10.2337/diacare.26.3.832
  contributor:
    fullname: MW Steffes
– volume: 42
  start-page: e116
  issue: 7
  year: 2019
  ident: 5708_CR24
  publication-title: Diabetes Care
  doi: 10.2337/dc18-2518
  contributor:
    fullname: S Yoneda
– volume: 8
  start-page: e001361
  issue: 2
  year: 2020
  ident: 5708_CR34
  publication-title: J Immunother Cancer
  doi: 10.1136/jitc-2020-001361
  contributor:
    fullname: A Cortellini
– volume: 104
  start-page: 5499
  issue: 11
  year: 2019
  ident: 5708_CR6
  publication-title: J Clin Endocrinol Metab
  doi: 10.1210/jc.2019-00423
  contributor:
    fullname: VHM Tsang
– volume: 52
  start-page: 1391
  issue: 7
  year: 2009
  ident: 5708_CR23
  publication-title: Diabetologia
  doi: 10.1007/s00125-009-1374-z
  contributor:
    fullname: AM Madec
SSID ssj0003546
Score 2.574533
Snippet Aims/hypothesis Immunomodulators blocking cytotoxic T-lymphocyte-associated protein 4 (CTLA-4) and programmed cell death protein 1 (PD-1) or programmed...
Immunomodulators blocking cytotoxic T-lymphocyte-associated protein 4 (CTLA-4) and programmed cell death protein 1 (PD-1) or programmed death-ligand 1 (PD-L1)...
Aims/hypothesisImmunomodulators blocking cytotoxic T-lymphocyte-associated protein 4 (CTLA-4) and programmed cell death protein 1 (PD-1) or programmed...
AIMS/HYPOTHESISImmunomodulators blocking cytotoxic T-lymphocyte-associated protein 4 (CTLA-4) and programmed cell death protein 1 (PD-1) or programmed...
SourceID pubmedcentral
proquest
crossref
pubmed
springer
SourceType Open Access Repository
Aggregation Database
Index Database
Publisher
StartPage 1185
SubjectTerms Animals
Antibodies, Monoclonal
Apoptosis
B7-H1 Antigen - metabolism
Beta cells
Cancer
Cancer therapies
CD3 antigen
Cell death
Chemokines
CTLA-4 protein
Cytokines
Cytotoxicity
Diabetes
Diabetes mellitus (insulin dependent)
Diabetes Mellitus, Type 1 - metabolism
Fibrosis
Human Physiology
Humans
Immune Checkpoint Inhibitors
Immune system
Immunofluorescence
Immunomodulation
Insulin
Internal Medicine
Ligands
Lymphocytes
Lymphocytes T
Macrophages
Male
Medicine
Medicine & Public Health
Mesenchymal stem cells
Mesenchymal Stem Cells - metabolism
Metabolic Diseases
Metastases
Mice
Mice, Inbred NOD
Monoclonal antibodies
Monocytes
Neoplasms - metabolism
Patients
PD-1 protein
PD-L1 protein
Plasma
Programmed Cell Death 1 Receptor - metabolism
Stem cells
Tumors
SummonAdditionalLinks – databaseName: ProQuest Central
  dbid: BENPR
  link: http://utb.summon.serialssolutions.com/2.0.0/link/0/eLvHCXMwfV3da9swED-6BMZeRj-2NesHGuxtE_O35afSlpZQaBijgbwZWZJpWmq7czrof987RXbIQvtqnbCt3-n000l3B_Bd4gbN16nPEx1qHkVeyTMhYu6JwqSoz75R9rbFJBlPo6tZPHMOt9Zdq-xsojXUulbkI_8VUEEV3KsI76R55FQ1ik5XXQmNdzAM_FCIAQzPLia___S2OHShOmiGuS-SmQubscFz9JCikwOOnIW8hOtL0wbf3Lw2-d_ZqV2SLrfho-OS7HQJ_g5smWoX3l-70_I9uLMeeib1vKlbwzUq2z-j2QMFHKnb5wfsS2mcGTnvW9Yskzkxcsoyn3VOWYabdoRfs-KZzSmYxDDEWd039RyFC1wL76U2n2B6eXFzPuautgJXcRYv0MYhkfGKCNHJZFooLzFlJhTimcqk1NRSIBmLSmVkWCRKlCrxtDAoLUOhVfgZBlVdmX1gKo2lTMNMRJIqq5eSAp1JNdBaeMiuRvCjG9a8WabQyPtkyRaEHEHILQg5Sh92I5-76dTmK_BH8K1vxolAAyQrUz-RTEJ0V6TBCL4sgepfh6QKeWUoRpCuQdgLUJLt9ZZqfmuTbWe0ZQuw588O7NVnvf4XX9_-iwP4EFjFo2u_hzBY_H0yR0huFsWx0-AXE_T4Cg
  priority: 102
  providerName: ProQuest
Title Human adipose-derived mesenchymal stem cells prevent type 1 diabetes induced by immune checkpoint blockade
URI https://link.springer.com/article/10.1007/s00125-022-05708-3
https://www.ncbi.nlm.nih.gov/pubmed/35511238
https://www.proquest.com/docview/2673710780
https://search.proquest.com/docview/2660099872
https://pubmed.ncbi.nlm.nih.gov/PMC9174328
Volume 65
hasFullText 1
inHoldings 1
isFullTextHit
isPrint
link http://utb.summon.serialssolutions.com/2.0.0/link/0/eLvHCXMwlV3dT9swED9BkdBe0GBjFLrKk_Y2LOXTdh67qoA2DSG0SuUpcmxHFERa0YLEf8-dmwR1jAdeEik-58O_i-_ns-8M8F3jAC20MuTCxpYnSVDyTKmUB6pwEvU5dMavtjgXZ-Pk1ySdvMRx-8XuzYyk76jbWDcyzBRMHHGkGOTU24QtJA8xJcwfR4O2-43r6BwU56ESkzpS5v_3WLdGryjm65WS_0yXeit08hF2avrIBiu8d2HDVXuw_aeeIP8EN94pz7SdzmcLxy3q16Oz7I5ijMz10x3WpczNjPz1CzZf5W9i5IdlIWv8sAzH6Yi4ZcUTm1L8iGMIrbmdz6YoXKD5u9XWfYbxyejv8IzX2ylwk2bpErs15C5BkSAgmZaFCYQrM2UQQqlFaamkQP6VlMbpuBBGlUYEVjmU1rGyJt6HTjWr3AEwI1OtZZypRNNm6qWm2GbSBuwgAiRUXfjRNGs-X2XNyNv8yB6EHEHIPQg5Sveals_rP2iRR7SBDo5NVdCFb20x6j41kK7c7IFkBDFcJaMufFkB1T4OeRRSyVh1Qa5B2ApQXu31kmp67fNrZzRKi7DmcQP2y2u9_RWH7xM_gg-RV0Ra-duDzvL-wX1FfrMs-rApJxKPahj2YWtwevV7hOefo_OLS7w6FMO-1_hnX1D4xg
link.rule.ids 230,314,780,784,885,12056,12223,21388,27924,27925,31719,31720,33266,33267,33744,33745,41081,41120,41523,42150,42189,42592,43310,43579,43805,51576,52111,52234,73745,74014,74302
linkProvider Springer Nature
linkToHtml http://utb.summon.serialssolutions.com/2.0.0/link/0/eLvHCXMwfV1LT9wwEB7xkIBLVaDAtpQaiRtYzdvOCSFUtJTHCaS9RY7tiAWRBHZB4t93xuvsaovgGk-UxN9k_Hk8D4ADhRu00IiQZyY2PEmCiudSpjyQpRWoz6HVLtriOuvfJn8H6cA73EY-rLKzic5Qm0aTj_x3RA1VcK8ig-P2iVPXKDpd9S00FmEZl31BWi1PZyEesU_UQSPMQ5kNfNKMS52ji5SbHHFkLOQjnF-Y3rHN90GT_52cugXp7Ct88UySnUygX4cFW2_AypU_K9-Ee-efZ8oM22ZkuUFVe7WGPVK6kb57e8R7qYgzI9f9iLWTUk6MXLIsZJ1LluGWHcE3rHxjQ0olsQxR1g9tM0ThElfCB2XsN7g9-3Nz2ue-swLXaZ6O0cIhjQnKBLHJlSh1kNkqlxrRFCqrDI2USMWSSlsVl5mWlc4CIy1Kq1gaHW_BUt3UdgeYFqlSIs5loqiveqUozZkUA21FgNyqB4fdtBbtpIBGMS2V7EAoEITCgVCg9G4384X_mUbFDPoe7E-H8TegCVK1bV5IJiOyK0XUg-0JUNPHIaVCVhnLHog5CKcCVGJ7fqQe3rlS2zlt2CK886gDe_ZaH3_F98-_4hes9m-uLovL8-uLH7AWOSWkAOBdWBo_v9ifSHPG5Z7T5X9ndPlg
linkToPdf http://utb.summon.serialssolutions.com/2.0.0/link/0/eLvHCXMwfV1ZT-MwEB5xSIgXxLEs5fRKvIFF7jhPCAEVx4J4AKlvkWM7oiCSQAsS_54Z12nVRctrPFESz5fx5_EcAPsSN2i-Tn2e6FDzKPJKngkRc08UJkU8-0bZaIvb5OIhuurFPRf_NHBhla1NtIZa14p85EcBNVTBvYrwjkoXFnF31j1uXjl1kKKTVtdOYxbmqcsc1dEXp5Nwj9Al7aBB5r5Iei6BxqbR0UXKUw44shfyF04vUt-Y5_cAyn9OUe3i1F2GJccq2ckIBiswY6pVWLhx5-Zr8GR99UzqflMPDNcIuw-j2QulHqnHzxe8lwo6M3LjD1gzKuvEyD3LfNa6Zxlu3xEImhWfrE9pJYahxtVzU_dRuMBV8Vlq8wseuuf3pxfcdVngKs7iIVo7pDReEaGeMpkWyktMmQmFmk1lUmoaKZCWRaUyMiwSJUqVeFoYlJah0Cpch7mqrswGMJXGUqZhJiJJPdZLSSnPBBK0Gx7yrA4ctNOaN6NiGvm4bLJVQo5KyK0ScpTebmc-dz_WIJ_AoAN_xsP4S9AEycrU7ySTEPEVadCB3yNFjR-H9AoZZig6kE6pcCxA5banR6r-oy27ndHmLcA7D1tlT17r_1-x-fNX7MECwjj_e3l7vQWLgcUgxQJvw9zw7d3sIOMZFrsWyl_55f2F
openUrl ctx_ver=Z39.88-2004&ctx_enc=info%3Aofi%2Fenc%3AUTF-8&rfr_id=info%3Asid%2Fsummon.serialssolutions.com&rft_val_fmt=info%3Aofi%2Ffmt%3Akev%3Amtx%3Ajournal&rft.genre=article&rft.atitle=Human+adipose-derived+mesenchymal+stem+cells+prevent+type+1+diabetes+induced+by+immune+checkpoint+blockade&rft.jtitle=Diabetologia&rft.au=Kawada-Horitani%2C+Emi&rft.au=Kita%2C+Shunbun&rft.au=Okita%2C+Tomonori&rft.au=Nakamura%2C+Yuto&rft.date=2022-07-01&rft.pub=Springer+Berlin+Heidelberg&rft.issn=0012-186X&rft.eissn=1432-0428&rft.volume=65&rft.issue=7&rft.spage=1185&rft.epage=1197&rft_id=info:doi/10.1007%2Fs00125-022-05708-3&rft_id=info%3Apmid%2F35511238&rft.externalDBID=PMC9174328
thumbnail_l http://covers-cdn.summon.serialssolutions.com/index.aspx?isbn=/lc.gif&issn=0012-186X&client=summon
thumbnail_m http://covers-cdn.summon.serialssolutions.com/index.aspx?isbn=/mc.gif&issn=0012-186X&client=summon
thumbnail_s http://covers-cdn.summon.serialssolutions.com/index.aspx?isbn=/sc.gif&issn=0012-186X&client=summon