CD153/CD30 signaling promotes age-dependent tertiary lymphoid tissue expansion and kidney injury

Tertiary lymphoid tissues (TLTs) facilitate local T and B cell interactions in chronically inflamed organs. However, the cells and molecular pathways that govern TLT formation are poorly defined. Here, we identified TNF superfamily CD153/CD30 signaling between 2 unique age-dependent lymphocyte subpo...

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Published inThe Journal of clinical investigation Vol. 132; no. 2
Main Authors Sato, Yuki, Oguchi, Akiko, Fukushima, Yuji, Masuda, Kyoko, Toriu, Naoya, Taniguchi, Keisuke, Yoshikawa, Takahisa, Cui, Xiaotong, Kondo, Makiko, Hosoi, Takeshi, Komidori, Shota, Shimizu, Yoko, Fujita, Harumi, Jiang, Li, Kong, Yingyi, Yamanashi, Takashi, Seita, Jun, Yamamoto, Takuya, Toyokuni, Shinya, Hamazaki, Yoko, Hattori, Masakazu, Yoshikai, Yasunobu, Boor, Peter, Floege, Jürgen, Kawamoto, Hiroshi, Murakawa, Yasuhiro, Minato, Nagahiro, Yanagita, Motoko
Format Journal Article
LanguageEnglish
Published United States American Society for Clinical Investigation 18.01.2022
Subjects
Acute Kidney Injury - genetics
Acute Kidney Injury - immunology
Age factors in disease
Aging - genetics
Aging - immunology
Animals
CD30 Ligand - genetics
CD30 Ligand - immunology
CD4-Positive T-Lymphocytes - immunology
Cellular signal transduction
Development and progression
Health aspects
Inflammation
Ki-1 Antigen - genetics
Ki-1 Antigen - immunology
Kidney diseases
Lymphoid tissue
Lymphoid Tissue - immunology
Male
Mice
Mice, Knockout
Nephrology
Signal Transduction - genetics
Signal Transduction - immunology
Tumor necrosis factor
Japan
Nephrology
Chronic kidney disease
Inflammation
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Abstract Tertiary lymphoid tissues (TLTs) facilitate local T and B cell interactions in chronically inflamed organs. However, the cells and molecular pathways that govern TLT formation are poorly defined. Here, we identified TNF superfamily CD153/CD30 signaling between 2 unique age-dependent lymphocyte subpopulations, CD153+PD-1+CD4+ senescence-associated T (SAT) cells and CD30+T-bet+ age-associated B cells (ABCs), as a driver for TLT expansion. SAT cells, which produced ABC-inducing factors IL-21 and IFN-γ, and ABCs progressively accumulated within TLTs in aged kidneys after injury. Notably, in kidney injury models, CD153 or CD30 deficiency impaired functional SAT cell induction, which resulted in reduced ABC numbers and attenuated TLT formation with improved inflammation, fibrosis, and renal function. Attenuated TLT formation after transplantation of CD153-deficient bone marrow further supported the importance of CD153 in immune cells. Clonal analysis revealed that SAT cells and ABCs in the kidneys arose from both local differentiation and recruitment from the spleen. In the synovium of aged rheumatoid arthritis patients, T peripheral helper/T follicular helper cells and ABCs also expressed CD153 and CD30, respectively. Together, our data reveal a previously unappreciated function of CD153/CD30 signaling in TLT formation and propose targeting the CD153/CD30 signaling pathway as a therapeutic target for slowing kidney disease progression.
AbstractList Tertiary lymphoid tissues (TLTs) facilitate local T and B cell interactions in chronically inflamed organs. However, the cells and molecular pathways that govern TLT formation are poorly defined. Here, we identified TNF superfamily CD153/CD30 signaling between 2 unique age-dependent lymphocyte subpopulations, CD153+PD-1+CD4+ senescence-associated T (SAT) cells and CD30+T-bet+ age-associated B cells (ABCs), as a driver for TLT expansion. SAT cells, which produced ABC-inducing factors IL-21 and IFN-γ, and ABCs progressively accumulated within TLTs in aged kidneys after injury. Notably, in kidney injury models, CD153 or CD30 deficiency impaired functional SAT cell induction, which resulted in reduced ABC numbers and attenuated TLT formation with improved inflammation, fibrosis, and renal function. Attenuated TLT formation after transplantation of CD153-deficient bone marrow further supported the importance of CD153 in immune cells. Clonal analysis revealed that SAT cells and ABCs in the kidneys arose from both local differentiation and recruitment from the spleen. In the synovium of aged rheumatoid arthritis patients, T peripheral helper/T follicular helper cells and ABCs also expressed CD153 and CD30, respectively. Together, our data reveal a previously unappreciated function of CD153/CD30 signaling in TLT formation and propose targeting the CD153/CD30 signaling pathway as a therapeutic target for slowing kidney disease progression.
Tertiary lymphoid tissues (TLTs) facilitate local T and B cell interactions in chronically inflamed organs. However, the cells and molecular pathways that govern TLT formation are poorly defined. Here, we identified TNF superfamily CD153/CD30 signaling between 2 unique age-dependent lymphocyte subpopulations, [CD153.sup.+][PD-1.sup.+][CD4.sup.+] senescence-associated T (SAT) cells and CD30+T-bet+ age-associated B cells (ABCs), as a driver for TLT expansion. SAT cells, which produced ABC-inducing factors IL-21 and IFN-[gamma], and ABCs progressively accumulated within TLTs in aged kidneys after injury. Notably, in kidney injury models, CD153 or CD30 deficiency impaired functional SAT cell induction, which resulted in reduced ABC numbers and attenuated TLT formation with improved inflammation, fibrosis, and renal function. Attenuated TLT formation after transplantation of CD153-deficient bone marrow further supported the importance of CD153 in immune cells. Clonal analysis revealed that SAT cells and ABCs in the kidneys arose from both local differentiation and recruitment from the spleen. In the synovium of aged rheumatoid arthritis patients, T peripheral helper/T follicular helper cells and ABCs also expressed CD153 and CD30, respectively. Together, our data reveal a previously unappreciated function of CD153/CD30 signaling in TLT formation and propose targeting the CD153/CD30 signaling pathway as a therapeutic target for slowing kidney disease progression.
Tertiary lymphoid tissues (TLTs) facilitate local T and B cell interactions in chronically inflamed organs. However, the cells and molecular pathways that govern TLT formation are poorly defined. Here, we identified TNF superfamily CD153/CD30 signaling between 2 unique age-dependent lymphocyte subpopulations, CD153 + PD-1 + CD4 + senescence-associated T (SAT) cells and CD30 + T-bet + age-associated B cells (ABCs), as a driver for TLT expansion. SAT cells, which produced ABC-inducing factors IL-21 and IFN-γ, and ABCs progressively accumulated within TLTs in aged kidneys after injury. Notably, in kidney injury models, CD153 or CD30 deficiency impaired functional SAT cell induction, which resulted in reduced ABC numbers and attenuated TLT formation with improved inflammation, fibrosis, and renal function. Attenuated TLT formation after transplantation of CD153-deficient bone marrow further supported the importance of CD153 in immune cells. Clonal analysis revealed that SAT cells and ABCs in the kidneys arose from both local differentiation and recruitment from the spleen. In the synovium of aged rheumatoid arthritis patients, T peripheral helper/T follicular helper cells and ABCs also expressed CD153 and CD30, respectively. Together, our data reveal a previously unappreciated function of CD153/CD30 signaling in TLT formation and propose targeting the CD153/CD30 signaling pathway as a therapeutic target for slowing kidney disease progression.
Tertiary lymphoid tissues (TLTs) facilitate local T and B cell interactions in chronically inflamed organs. However, the cells and molecular pathways that govern TLT formation are poorly defined. Here, we identified TNF superfamily CD153/CD30 signaling between 2 unique age-dependent lymphocyte subpopulations, CD153+PD-1+CD4+ senescence-associated T (SAT) cells and CD30+T-bet+ age-associated B cells (ABCs), as a driver for TLT expansion. SAT cells, which produced ABC-inducing factors IL-21 and IFN-γ, and ABCs progressively accumulated within TLTs in aged kidneys after injury. Notably, in kidney injury models, CD153 or CD30 deficiency impaired functional SAT cell induction, which resulted in reduced ABC numbers and attenuated TLT formation with improved inflammation, fibrosis, and renal function. Attenuated TLT formation after transplantation of CD153-deficient bone marrow further supported the importance of CD153 in immune cells. Clonal analysis revealed that SAT cells and ABCs in the kidneys arose from both local differentiation and recruitment from the spleen. In the synovium of aged rheumatoid arthritis patients, T peripheral helper/T follicular helper cells and ABCs also expressed CD153 and CD30, respectively. Together, our data reveal a previously unappreciated function of CD153/CD30 signaling in TLT formation and propose targeting the CD153/CD30 signaling pathway as a therapeutic target for slowing kidney disease progression.Tertiary lymphoid tissues (TLTs) facilitate local T and B cell interactions in chronically inflamed organs. However, the cells and molecular pathways that govern TLT formation are poorly defined. Here, we identified TNF superfamily CD153/CD30 signaling between 2 unique age-dependent lymphocyte subpopulations, CD153+PD-1+CD4+ senescence-associated T (SAT) cells and CD30+T-bet+ age-associated B cells (ABCs), as a driver for TLT expansion. SAT cells, which produced ABC-inducing factors IL-21 and IFN-γ, and ABCs progressively accumulated within TLTs in aged kidneys after injury. Notably, in kidney injury models, CD153 or CD30 deficiency impaired functional SAT cell induction, which resulted in reduced ABC numbers and attenuated TLT formation with improved inflammation, fibrosis, and renal function. Attenuated TLT formation after transplantation of CD153-deficient bone marrow further supported the importance of CD153 in immune cells. Clonal analysis revealed that SAT cells and ABCs in the kidneys arose from both local differentiation and recruitment from the spleen. In the synovium of aged rheumatoid arthritis patients, T peripheral helper/T follicular helper cells and ABCs also expressed CD153 and CD30, respectively. Together, our data reveal a previously unappreciated function of CD153/CD30 signaling in TLT formation and propose targeting the CD153/CD30 signaling pathway as a therapeutic target for slowing kidney disease progression.
Audience Academic
Author Minato, Nagahiro
Toriu, Naoya
Yamamoto, Takuya
Yanagita, Motoko
Masuda, Kyoko
Kong, Yingyi
Hamazaki, Yoko
Kawamoto, Hiroshi
Yoshikawa, Takahisa
Floege, Jürgen
Yoshikai, Yasunobu
Murakawa, Yasuhiro
Oguchi, Akiko
Cui, Xiaotong
Yamanashi, Takashi
Hosoi, Takeshi
Sato, Yuki
Kondo, Makiko
Shimizu, Yoko
Boor, Peter
Fukushima, Yuji
Hattori, Masakazu
Seita, Jun
Jiang, Li
Taniguchi, Keisuke
Komidori, Shota
Fujita, Harumi
Toyokuni, Shinya
AuthorAffiliation 17 DSK Project, Graduate School of Medicine, Kyoto University, Kyoto, Japan
4 Department of Immunosenescence and
8 Department of Pathology and Biological Responses, Nagoya University Graduate School of Medicine, Nagoya, Aichi, Japan
15 Institute of Pathology and
16 Department of Nephrology, RWTH University of Aachen, Aachen, Germany
5 Department of Immunology and Cell Biology, Graduate School of Medicine, Kyoto University, Kyoto, Japan
14 Division of Host Defense, Network Center for Infectious Disease, Medical Institute of Bioregulation, Kyushu University, Fukuoka, Japan
9 Medical Sciences Innovation Hub Program, RIKEN, Tokyo, Japan
1 Department of Nephrology
11 Medical-risk Avoidance Based on iPS Cells Team, RIKEN Center for Advanced Intelligence Project (AIP), Kyoto, Japan
13 Laboratory of Immunobiology, Center for iPS Cell Research and Application (CiRA), Kyoto University, Kyoto, Japan
6 Department of Immunology, Institute for Frontier Medical Science, and
7 Institute for the Advanced Study of
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BackLink https://www.ncbi.nlm.nih.gov/pubmed/34813503$$D View this record in MEDLINE/PubMed
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2022 Sato et al. 2022 Sato et al.
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Issue 2
Keywords Nephrology
Chronic kidney disease
Inflammation
Language English
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Snippet Tertiary lymphoid tissues (TLTs) facilitate local T and B cell interactions in chronically inflamed organs. However, the cells and molecular pathways that...
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SubjectTerms Acute Kidney Injury - genetics
Acute Kidney Injury - immunology
Age factors in disease
Aging - genetics
Aging - immunology
Animals
CD30 Ligand - genetics
CD30 Ligand - immunology
CD4-Positive T-Lymphocytes - immunology
Cellular signal transduction
Development and progression
Health aspects
Inflammation
Ki-1 Antigen - genetics
Ki-1 Antigen - immunology
Kidney diseases
Lymphoid tissue
Lymphoid Tissue - immunology
Male
Mice
Mice, Knockout
Nephrology
Signal Transduction - genetics
Signal Transduction - immunology
Tumor necrosis factor
Title CD153/CD30 signaling promotes age-dependent tertiary lymphoid tissue expansion and kidney injury
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Volume 132
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