Role of interleukin‐1β in NLRP12‐associated autoinflammatory disorders and resistance to anti–interleukin‐1 therapy

Objective A new class of autoinflammatory syndromes called NLRP12‐associated disorders (NLRP12AD) has been associated with mutations in NLRP12. Conflicting data on the putative role of NLRP12 in interleukin‐1β (IL‐1β) signaling have been found in in vitro analyses. This prospective study was underta...

Full description

Saved in:
Bibliographic Details
Published inArthritis & rheumatology (Hoboken, N.J.) Vol. 63; no. 7; pp. 2142 - 2148
Main Authors Jéru, Isabelle, Hentgen, Véronique, Normand, Sylvain, Duquesnoy, Philippe, Cochet, Emmanuelle, Delwail, Adriana, Grateau, Gilles, Marlin, Sandrine, Amselem, Serge, Lecron, Jean‐Claude
Format Journal Article
LanguageEnglish
Published Hoboken Wiley Subscription Services, Inc., A Wiley Company 01.07.2011
Wiley
Subjects
Online AccessGet full text

Cover

Loading…
Abstract Objective A new class of autoinflammatory syndromes called NLRP12‐associated disorders (NLRP12AD) has been associated with mutations in NLRP12. Conflicting data on the putative role of NLRP12 in interleukin‐1β (IL‐1β) signaling have been found in in vitro analyses. This prospective study was undertaken to assess the secretion of IL‐1β and 3 IL‐1β–induced cytokines (IL‐1 receptor antagonist [IL‐1Ra], IL‐6, and tumor necrosis factor α [TNFα]) in patients' peripheral blood mononuclear cells (PBMCs) cultured ex vivo and to evaluate the patients' response to IL‐1Ra (anakinra), a major drug used in the treatment of autoinflammatory disorders. Methods Patients' disease manifestations and cytokine measurements were recorded before anakinra treatment was started, during 14 months of therapy, and after discontinuation of anakinra treatment. Results Spontaneous secretion of IL‐1β by patients' PBMCs was found to be dramatically increased (80–175 fold) compared to healthy controls. Consistent with these findings, anakinra initially led to a marked clinical improvement and to a rapid near‐normalization of IL‐1β secretion. However, a progressive clinical relapse occurred secondarily, associated with an increase in TNFα secretion, persistent elevated levels of IL‐1Ra and IL‐6, and a reactivation of IL‐1β secretion. Anakinra was discontinued after 14 months of therapy. Conclusion Our findings provide in vivo evidence of the crucial role of IL‐1β in the pathophysiology of NLRP12AD. This is the first time anakinra has been used to treat this disorder. This study provides new insights into the mechanisms underlying resistance to anti–IL‐1 therapy observed in a few patients with autoinflammatory syndromes. Our data also point to the potential of ex vivo cytokine measurements as predictors of response to treatment.
AbstractList OBJECTIVEA new class of autoinflammatory syndromes called NLRP12-associated disorders (NLRP12AD) has been associated with mutations in NLRP12. Conflicting data on the putative role of NLRP12 in interleukin-1β (IL-1β) signaling have been found in in vitro analyses. This prospective study was undertaken to assess the secretion of IL-1β and 3 IL-1β-induced cytokines (IL-1 receptor antagonist [IL-1Ra], IL-6, and tumor necrosis factor α [TNFα]) in patients' peripheral blood mononuclear cells (PBMCs) cultured ex vivo and to evaluate the patients' response to IL-1Ra (anakinra), a major drug used in the treatment of autoinflammatory disorders.METHODSPatients' disease manifestations and cytokine measurements were recorded before anakinra treatment was started, during 14 months of therapy, and after discontinuation of anakinra treatment.RESULTSSpontaneous secretion of IL-1β by patients' PBMCs was found to be dramatically increased (80-175 fold) compared to healthy controls. Consistent with these findings, anakinra initially led to a marked clinical improvement and to a rapid near-normalization of IL-1β secretion. However, a progressive clinical relapse occurred secondarily, associated with an increase in TNFα secretion, persistent elevated levels of IL-1Ra and IL-6, and a reactivation of IL-1β secretion. Anakinra was discontinued after 14 months of therapy.CONCLUSIONOur findings provide in vivo evidence of the crucial role of IL-1β in the pathophysiology of NLRP12AD. This is the first time anakinra has been used to treat this disorder. This study provides new insights into the mechanisms underlying resistance to anti-IL-1 therapy observed in a few patients with autoinflammatory syndromes. Our data also point to the potential of ex vivo cytokine measurements as predictors of response to treatment.
A new class of autoinflammatory syndromes called NLRP12-associated disorders (NLRP12AD) has been associated with mutations in NLRP12. Conflicting data on the putative role of NLRP12 in interleukin-1β (IL-1β) signaling have been found in in vitro analyses. This prospective study was undertaken to assess the secretion of IL-1β and 3 IL-1β-induced cytokines (IL-1 receptor antagonist [IL-1Ra], IL-6, and tumor necrosis factor α [TNFα]) in patients' peripheral blood mononuclear cells (PBMCs) cultured ex vivo and to evaluate the patients' response to IL-1Ra (anakinra), a major drug used in the treatment of autoinflammatory disorders. Patients' disease manifestations and cytokine measurements were recorded before anakinra treatment was started, during 14 months of therapy, and after discontinuation of anakinra treatment. Spontaneous secretion of IL-1β by patients' PBMCs was found to be dramatically increased (80-175 fold) compared to healthy controls. Consistent with these findings, anakinra initially led to a marked clinical improvement and to a rapid near-normalization of IL-1β secretion. However, a progressive clinical relapse occurred secondarily, associated with an increase in TNFα secretion, persistent elevated levels of IL-1Ra and IL-6, and a reactivation of IL-1β secretion. Anakinra was discontinued after 14 months of therapy. Our findings provide in vivo evidence of the crucial role of IL-1β in the pathophysiology of NLRP12AD. This is the first time anakinra has been used to treat this disorder. This study provides new insights into the mechanisms underlying resistance to anti-IL-1 therapy observed in a few patients with autoinflammatory syndromes. Our data also point to the potential of ex vivo cytokine measurements as predictors of response to treatment.
Objective: A new class of autoinflammatory syndromes called NLRP12-associated disorders (NLRP12AD) has been associated with mutations in NLRP12. Conflicting data on the putative role of NLRP12 in interleukin-1β (IL-1β) signaling have been found in in vitro analyses. This prospective study was undertaken to assess the secretion of IL-1β and 3 IL-1β-induced cytokines (IL-1 receptor antagonist [IL-1Ra], IL-6, and tumor necrosis factor α [TNFα]) in patients' peripheral blood mononuclear cells (PBMCs) cultured ex vivo and to evaluate the patients' response to IL-1Ra (anakinra), a major drug used in the treatment of autoinflammatory disorders.Methods: Patients' disease manifestations and cytokine measurements were recorded before anakinra treatment was started, during 14 months of therapy, and after discontinuation of anakinra treatment.Results: Spontaneous secretion of IL-1β by patients' PBMCs was found to be dramatically increased (80-175 fold) compared to healthy controls. Consistent with these findings, anakinra initially led to a marked clinical improvement and to a rapid near-normalization of IL-1β secretion. However, a progressive clinical relapse occurred secondarily, associated with an increase in TNFα secretion, persistent elevated levels of IL-1Ra and IL-6, and a reactivation of IL-1β secretion. Anakinra was discontinued after 14 months of therapy.Conclusion: Our findings provide in vivo evidence of the crucial role of IL-1β in the pathophysiology of NLRP12AD. This is the first time anakinra has been used to treat this disorder. This study provides new insights into the mechanisms underlying resistance to anti-IL-1 therapy observed in a few patients with autoinflammatory syndromes. Our data also point to the potential of ex vivo cytokine measurements as predictors of response to treatment.
Objective A new class of autoinflammatory syndromes called NLRP12‐associated disorders (NLRP12AD) has been associated with mutations in NLRP12. Conflicting data on the putative role of NLRP12 in interleukin‐1β (IL‐1β) signaling have been found in in vitro analyses. This prospective study was undertaken to assess the secretion of IL‐1β and 3 IL‐1β–induced cytokines (IL‐1 receptor antagonist [IL‐1Ra], IL‐6, and tumor necrosis factor α [TNFα]) in patients' peripheral blood mononuclear cells (PBMCs) cultured ex vivo and to evaluate the patients' response to IL‐1Ra (anakinra), a major drug used in the treatment of autoinflammatory disorders. Methods Patients' disease manifestations and cytokine measurements were recorded before anakinra treatment was started, during 14 months of therapy, and after discontinuation of anakinra treatment. Results Spontaneous secretion of IL‐1β by patients' PBMCs was found to be dramatically increased (80–175 fold) compared to healthy controls. Consistent with these findings, anakinra initially led to a marked clinical improvement and to a rapid near‐normalization of IL‐1β secretion. However, a progressive clinical relapse occurred secondarily, associated with an increase in TNFα secretion, persistent elevated levels of IL‐1Ra and IL‐6, and a reactivation of IL‐1β secretion. Anakinra was discontinued after 14 months of therapy. Conclusion Our findings provide in vivo evidence of the crucial role of IL‐1β in the pathophysiology of NLRP12AD. This is the first time anakinra has been used to treat this disorder. This study provides new insights into the mechanisms underlying resistance to anti–IL‐1 therapy observed in a few patients with autoinflammatory syndromes. Our data also point to the potential of ex vivo cytokine measurements as predictors of response to treatment.
Author Hentgen, Véronique
Duquesnoy, Philippe
Delwail, Adriana
Cochet, Emmanuelle
Jéru, Isabelle
Grateau, Gilles
Lecron, Jean‐Claude
Normand, Sylvain
Marlin, Sandrine
Amselem, Serge
Author_xml – sequence: 1
  givenname: Isabelle
  surname: Jéru
  fullname: Jéru, Isabelle
– sequence: 2
  givenname: Véronique
  surname: Hentgen
  fullname: Hentgen, Véronique
– sequence: 3
  givenname: Sylvain
  surname: Normand
  fullname: Normand, Sylvain
– sequence: 4
  givenname: Philippe
  surname: Duquesnoy
  fullname: Duquesnoy, Philippe
– sequence: 5
  givenname: Emmanuelle
  surname: Cochet
  fullname: Cochet, Emmanuelle
– sequence: 6
  givenname: Adriana
  surname: Delwail
  fullname: Delwail, Adriana
– sequence: 7
  givenname: Gilles
  surname: Grateau
  fullname: Grateau, Gilles
– sequence: 8
  givenname: Sandrine
  surname: Marlin
  fullname: Marlin, Sandrine
– sequence: 9
  givenname: Serge
  surname: Amselem
  fullname: Amselem, Serge
  email: serge.amselem@trs.aphp.fr
– sequence: 10
  givenname: Jean‐Claude
  surname: Lecron
  fullname: Lecron, Jean‐Claude
BackLink http://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=24358172$$DView record in Pascal Francis
https://www.ncbi.nlm.nih.gov/pubmed/21480187$$D View this record in MEDLINE/PubMed
https://inserm.hal.science/inserm-03894153$$DView record in HAL
BookMark eNp1kcFqFEEQhhtJMJvowReQvogImaSre2a257gENcKissRzUztTQ1pnptfunsiChzyC4Jv4IHmIPImdzBpB8FT8VR__D_Ufsr3BDcTYMxAnIIQ8RR9PlFBz_YjNoJBVJkDBHpsJIfJMFRUcsMMQPicpVaEeswMJuRag5zP2feU64q7ldojkOxq_2OH2-gfc_Eob_n65-ggyaQzB1RYjNRzH6OzQdtj3GJ3f8sYG5xvygePQcE_BhohDTTy6tIn29vrnP-Y8XpLHzfYJ22-xC_R0N4_YpzevL87Os-WHt-_OFsusVhXorIJWEoAqapkTaUTZoFgrVA22a5lOeV1iS6IUuqhqSbrMAdsKVKOpElWpjtjx5HuJndl426PfGofWnC-Wxg6BfG-E0lUOhbqChL-c8I13X0cK0fQ21NR1OJAbg9HzPNeyVDKRryay9i4ET-2DOwhzV41J1Zj7ahL7fOc6rntqHsg_XSTgxQ7AUGPX-vREG_5yuSo0zO9CTyfum-1o-_9Es1hdTNG_ASx2rJE
CODEN ARHEAW
CitedBy_id crossref_primary_10_1038_ejhg_2014_257
crossref_primary_10_1002_art_37882
crossref_primary_10_1038_ni_2237
crossref_primary_10_1371_journal_pone_0156981
crossref_primary_10_1016_j_pcl_2016_08_008
crossref_primary_10_1007_s00296_018_4092_3
crossref_primary_10_1172_JCI166295
crossref_primary_10_3388_jspaci_34_253
crossref_primary_10_1016_j_berh_2012_07_009
crossref_primary_10_1093_rheumatology_keu170
crossref_primary_10_1007_s10620_019_05525_6
crossref_primary_10_1136_rmdopen_2023_003598
crossref_primary_10_1016_j_revmed_2018_01_004
crossref_primary_10_1101_cshperspect_a028563
crossref_primary_10_1016_j_arcped_2017_12_001
crossref_primary_10_1016_j_jaip_2018_05_006
crossref_primary_10_3390_ijms21020496
crossref_primary_10_1016_j_autrev_2014_08_001
crossref_primary_10_1136_jmedgenet_2013_101577
crossref_primary_10_1016_j_pharmthera_2018_02_011
crossref_primary_10_1016_j_clim_2013_04_008
crossref_primary_10_1189_jlb_3RU0514_265RR
crossref_primary_10_1371_journal_pone_0190547
crossref_primary_10_1111_1756_185X_12722
crossref_primary_10_3389_fimmu_2014_00169
crossref_primary_10_1124_pr_112_006171
crossref_primary_10_3389_fimmu_2019_02448
crossref_primary_10_1097_BOR_0b013e32835689b9
crossref_primary_10_1111_imr_12898
crossref_primary_10_1016_j_imlet_2017_11_013
crossref_primary_10_1111_febs_16203
crossref_primary_10_1007_s10067_014_2721_0
crossref_primary_10_1007_s12519_019_00294_8
crossref_primary_10_1371_journal_ppat_1003885
crossref_primary_10_1186_s43556_024_00179_x
crossref_primary_10_3389_fimmu_2020_588322
crossref_primary_10_1016_j_immuni_2012_07_006
crossref_primary_10_1155_2014_948154
crossref_primary_10_1155_2013_513782
crossref_primary_10_1016_j_clim_2014_07_003
crossref_primary_10_1016_j_pcl_2012_03_005
crossref_primary_10_1146_annurev_pathol_012414_040431
crossref_primary_10_3389_fimmu_2023_1321370
crossref_primary_10_1016_j_smim_2013_10_008
crossref_primary_10_1007_s10067_016_3410_y
crossref_primary_10_1016_j_jaci_2020_08_017
crossref_primary_10_1038_s41577_023_00849_x
crossref_primary_10_7554_eLife_40396
crossref_primary_10_1016_j_cytogfr_2016_11_001
crossref_primary_10_1016_j_jaip_2023_05_040
crossref_primary_10_1016_j_autrev_2012_07_027
crossref_primary_10_1016_j_jaci_2016_05_010
crossref_primary_10_1097_BOR_0b013e32834dd2d5
crossref_primary_10_1136_annrheumdis_2021_220977
crossref_primary_10_1084_jem_20181892
crossref_primary_10_3389_fphar_2018_01157
crossref_primary_10_1155_2013_939847
crossref_primary_10_1016_j_revmed_2016_10_053
crossref_primary_10_1038_s41598_017_04286_4
crossref_primary_10_1111_j_1600_065X_2011_01050_x
crossref_primary_10_1186_s13256_022_03404_9
crossref_primary_10_1016_j_cyto_2014_06_012
crossref_primary_10_1371_journal_pgen_1007005
crossref_primary_10_1016_j_jaci_2015_04_049
crossref_primary_10_1016_j_jtauto_2019_100031
crossref_primary_10_1042_CS20171498
crossref_primary_10_47360_1995_4484_2022_280_298
crossref_primary_10_1093_rheumatology_keaa304
crossref_primary_10_1186_s12969_022_00669_8
crossref_primary_10_1096_fj_202000795R
Cites_doi 10.1002/art.30105
10.1002/art.30170
10.1002/art.21965
10.1002/art.30241
10.1074/jbc.M502820200
10.1073/pnas.0708616105
10.1002/art.10870
10.1002/art.22842
10.1056/NEJMoa055137
10.1074/jbc.M203915200
10.4049/jimmunol.1002227
ContentType Journal Article
Copyright Copyright © 2011 by the American College of Rheumatology
2015 INIST-CNRS
Copyright © 2011 by the American College of Rheumatology.
Distributed under a Creative Commons Attribution 4.0 International License
Copyright_xml – notice: Copyright © 2011 by the American College of Rheumatology
– notice: 2015 INIST-CNRS
– notice: Copyright © 2011 by the American College of Rheumatology.
– notice: Distributed under a Creative Commons Attribution 4.0 International License
DBID IQODW
CGR
CUY
CVF
ECM
EIF
NPM
AAYXX
CITATION
7X8
1XC
DOI 10.1002/art.30378
DatabaseName Pascal-Francis
Medline
MEDLINE
MEDLINE (Ovid)
MEDLINE
MEDLINE
PubMed
CrossRef
MEDLINE - Academic
Hyper Article en Ligne (HAL)
DatabaseTitle MEDLINE
Medline Complete
MEDLINE with Full Text
PubMed
MEDLINE (Ovid)
CrossRef
MEDLINE - Academic
DatabaseTitleList MEDLINE - Academic
MEDLINE


Database_xml – sequence: 1
  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: 2
  dbid: EIF
  name: MEDLINE
  url: https://proxy.k.utb.cz/login?url=https://www.webofscience.com/wos/medline/basic-search
  sourceTypes: Index Database
DeliveryMethod fulltext_linktorsrc
Discipline Medicine
EISSN 1529-0131
2326-5191
EndPage 2148
ExternalDocumentID oai_HAL_inserm_03894153v1
10_1002_art_30378
21480187
24358172
ART30378
Genre article
Research Support, Non-U.S. Gov't
Journal Article
GrantInformation_xml – fundername: European Union Sixth Framework Programme (EURAMY project grant)
  funderid: LSHM‐CT‐2006‐037525
– fundername: Agence Nationale pour la Recherche
  funderid: 06‐MRAR‐010‐02
GroupedDBID ---
.3N
.55
.GA
.GJ
.Y3
05W
10A
1CY
1KJ
1L6
1OB
1OC
1ZS
23N
24P
31~
33P
3O-
3WU
4.4
4ZD
50Y
50Z
51W
51X
52M
52N
52O
52P
52R
52S
52T
52W
52X
53G
5GY
5RE
66C
6J9
6P2
702
7PT
8-0
8-1
8-3
8-4
8-5
8UM
930
A01
A03
AAEVG
AAHHS
AAKAS
AANLZ
AAQQT
AAWTL
AAXRX
AAZKR
ABCQN
ABCUV
ABEML
ABIJN
ABJNI
ABQWH
ABXGK
ACAHQ
ACBWZ
ACCFJ
ACCZN
ACFBH
ACGFO
ACMXC
ACPOU
ACSCC
ACXBN
ACXQS
ADBTR
ADEOM
ADIZJ
ADMGS
ADOZA
ADZCM
ADZOD
AEEZP
AEIGN
AEIMD
AEQDE
AEUQT
AEUYR
AFBPY
AFFNX
AFFPM
AFGKR
AFPWT
AFZJQ
AHBTC
AI.
AIACR
AITYG
AIURR
AIWBW
AJBDE
ALMA_UNASSIGNED_HOLDINGS
ALUQN
AMBMR
AMYDB
ASPBG
ATUGU
AVWKF
AZFZN
BDRZF
BROTX
BRXPI
BY8
C45
CS3
D-6
D-7
D-E
D-F
DCZOG
DPXWK
DR2
DRFUL
DRMAN
DRSTM
EBS
EJD
EMOBN
EX3
F00
F01
F04
F5P
FEDTE
G-S
G.N
GNP
GODZA
HBH
HF~
HGLYW
HHY
HHZ
HVGLF
HZ~
IX1
J5H
JPC
KQQ
LATKE
LAW
LC2
LC3
LEEKS
LH4
LITHE
LOXES
LP6
LP7
LSO
LUTES
LW6
LYRES
M65
MEWTI
MJL
MK4
MRFUL
MRMAN
MRSTM
MSFUL
MSMAN
MSSTM
MXFUL
MXMAN
MXSTM
N04
N05
N4W
N9A
NNB
OIG
OK1
OVD
P2P
P2W
P2X
P2Z
P4B
P4D
Q11
QB0
QRW
RGB
RIWAO
RJQFR
ROL
RWI
RX1
RXW
RYL
SAMSI
SJN
SUPJJ
SV3
TAE
TEORI
TWZ
UB1
V2E
V8K
V9Y
VH1
W8V
WH7
WIB
WIH
WIJ
WIK
WIN
WJL
WOW
WQJ
WRC
WUP
WXI
WXSBR
X6Y
X7M
XG1
XPP
XV2
YFH
YOC
ZGI
ZXP
ZZTAW
~IA
~WT
08R
AAUGY
AAVGM
ABHUG
ABPTK
ABWRO
ACXME
ADAWD
ADDAD
AFVGU
AGJLS
IQODW
ZA5
CGR
CUY
CVF
ECM
EIF
NPM
AAMNL
AAYXX
ACRPL
ACYXJ
CITATION
7X8
0R~
1XC
3SF
52U
52V
5VS
AAESR
AASGY
ABLJU
ABPVW
ACGFS
ACGOF
ACIWK
ACPRK
ADBBV
ADKYN
ADXAS
ADZMN
AENEX
AFRAH
AHMBA
ALAGY
AZVAB
BFHJK
BHBCM
BMXJE
DIK
FUBAC
KBYEO
NF~
O66
O9-
PQQKQ
WBKPD
WHWMO
WOHZO
WVDHM
YCJ
ID FETCH-LOGICAL-c3918-91f2e1135c24ee8aa2da0b3a3dafb22e14c6afe060859c2e8641af913d8e90963
IEDL.DBID DR2
ISSN 0004-3591
2326-5205
IngestDate Tue Oct 15 15:43:14 EDT 2024
Tue Dec 03 23:01:13 EST 2024
Fri Dec 06 01:30:36 EST 2024
Sat Sep 28 07:58:55 EDT 2024
Sun Oct 22 16:08:59 EDT 2023
Sat Aug 24 01:02:33 EDT 2024
IsPeerReviewed true
IsScholarly true
Issue 7
Keywords Resistance
Interleukin 1β
Treatment
Interleukin 1
Rheumatology
Language English
License CC BY 4.0
Copyright © 2011 by the American College of Rheumatology.
http://doi.wiley.com/10.1002/tdm_license_1
Distributed under a Creative Commons Attribution 4.0 International License: http://creativecommons.org/licenses/by/4.0
LinkModel DirectLink
MergedId FETCHMERGED-LOGICAL-c3918-91f2e1135c24ee8aa2da0b3a3dafb22e14c6afe060859c2e8641af913d8e90963
Notes Dr. Grateau has received consulting fees, speaking fees, and/or honoraria from Novartis (less than $10,000).
ObjectType-Article-1
SourceType-Scholarly Journals-1
ObjectType-Feature-2
content type line 23
ORCID 0000-0001-9506-3968
0000-0003-3990-5213
PMID 21480187
PQID 874482632
PQPubID 23479
PageCount 7
ParticipantIDs hal_primary_oai_HAL_inserm_03894153v1
proquest_miscellaneous_874482632
crossref_primary_10_1002_art_30378
pubmed_primary_21480187
pascalfrancis_primary_24358172
wiley_primary_10_1002_art_30378_ART30378
PublicationCentury 2000
PublicationDate July 2011
PublicationDateYYYYMMDD 2011-07-01
PublicationDate_xml – month: 07
  year: 2011
  text: July 2011
PublicationDecade 2010
PublicationPlace Hoboken
PublicationPlace_xml – name: Hoboken
– name: Hoboken , NJ
– name: United States
PublicationTitle Arthritis & rheumatology (Hoboken, N.J.)
PublicationTitleAlternate Arthritis Rheum
PublicationYear 2011
Publisher Wiley Subscription Services, Inc., A Wiley Company
Wiley
Publisher_xml – name: Wiley Subscription Services, Inc., A Wiley Company
– name: Wiley
References 2011; 63
2005; 280
2010; 185
2003; 48
2008; 105
2006; 54
2007; 56
2006; 355
2002; 277
Wang (10.1002/art.30378-BIB6|cit6) 2002; 277
Fleischmann (10.1002/art.30378-BIB11|cit11) 2003; 48
Jeru (10.1002/art.30378-BIB5|cit5) 2011; 63
Arthur (10.1002/art.30378-BIB8|cit8) 2010; 185
Lachmann (10.1002/art.30378-BIB3|cit3) 2011; 63
Goldbach-Mansky (10.1002/art.30378-BIB1|cit1) 2006; 355
Gattorno (10.1002/art.30378-BIB2|cit2) 2007; 56
Jeru (10.1002/art.30378-BIB4|cit4) 2008; 105
Matsubara (10.1002/art.30378-BIB10|cit10) 2006; 54
Borghini (10.1002/art.30378-BIB9|cit9) 2011; 63
Williams (10.1002/art.30378-BIB7|cit7) 2005; 280
References_xml – volume: 105
  start-page: 1614
  year: 2008
  end-page: 9
  article-title: Mutations in NALP12 cause hereditary periodic fever syndromes
  publication-title: Proc Natl Acad Sci U S A
– volume: 185
  start-page: 4515
  year: 2010
  end-page: 9
  article-title: Cutting edge: NLRP12 controls dendritic and myeloid cell migration to affect contact hypersensitivity
  publication-title: J Immunol
– volume: 63
  start-page: 1459
  year: 2011
  end-page: 64
  article-title: Identification and functional consequences of a recurrent NLRP12 missense mutation in periodic fever syndromes
  publication-title: Arthritis Rheum
– volume: 280
  start-page: 39914
  year: 2005
  end-page: 24
  article-title: The CATERPILLER protein Monarch‐1 is an antagonist of Toll‐like receptor‐, tumor necrosis factor α‐, and Mycobacterium tuberculosis‐induced pro‐inflammatory signals
  publication-title: J Biol Chem
– volume: 355
  start-page: 581
  year: 2006
  end-page: 92
  article-title: Neonatal‐onset multisystem inflammatory disease responsive to interleukin‐1β inhibition
  publication-title: N Engl J Med
– volume: 48
  start-page: 927
  year: 2003
  end-page: 34
  article-title: Anakinra, a recombinant human interleukin‐1 receptor antagonist (r‐metHuIL‐1ra), in patients with rheumatoid arthritis: a large, international, multicenter, placebo‐controlled trial
  publication-title: Arthritis Rheum
– volume: 63
  start-page: 314
  year: 2011
  end-page: 24
  article-title: The emerging role of interleukin‐1β in autoinflammatory diseases
  publication-title: Arthritis Rheum
– volume: 277
  start-page: 29874
  year: 2002
  end-page: 80
  article-title: PYPAF7, a novel PYRIN‐containing Apaf1‐like protein that regulates activation of NF‐κB and caspase‐1‐dependent cytokine processing
  publication-title: J Biol Chem
– volume: 54
  start-page: 2314
  year: 2006
  end-page: 20
  article-title: A severe case of chronic infantile neurologic, cutaneous, articular syndrome treated with biologic agents
  publication-title: Arthritis Rheum
– volume: 56
  start-page: 3138
  year: 2007
  end-page: 48
  article-title: Pattern of interleukin‐1β secretion in response to lipopolysaccharide and ATP before and after interleukin‐1 blockade in patients with CIAS1 mutations
  publication-title: Arthritis Rheum
– volume: 63
  start-page: 830
  year: 2011
  end-page: 9
  article-title: Clinical presentation and pathogenesis of cold‐induced autoinflammatory disease in a family with recurrence of an NLRP12 mutation
  publication-title: Arthritis Rheum
– volume: 63
  start-page: 314
  year: 2011
  ident: 10.1002/art.30378-BIB3|cit3
  article-title: The emerging role of interleukin-1β in autoinflammatory diseases
  publication-title: Arthritis Rheum
  doi: 10.1002/art.30105
  contributor:
    fullname: Lachmann
– volume: 63
  start-page: 830
  year: 2011
  ident: 10.1002/art.30378-BIB9|cit9
  article-title: Clinical presentation and pathogenesis of cold-induced autoinflammatory disease in a family with recurrence of an NLRP12 mutation
  publication-title: Arthritis Rheum
  doi: 10.1002/art.30170
  contributor:
    fullname: Borghini
– volume: 54
  start-page: 2314
  year: 2006
  ident: 10.1002/art.30378-BIB10|cit10
  article-title: A severe case of chronic infantile neurologic, cutaneous, articular syndrome treated with biologic agents
  publication-title: Arthritis Rheum
  doi: 10.1002/art.21965
  contributor:
    fullname: Matsubara
– volume: 63
  start-page: 1459
  year: 2011
  ident: 10.1002/art.30378-BIB5|cit5
  article-title: Identification and functional consequences of a recurrent NLRP12 missense mutation in periodic fever syndromes
  publication-title: Arthritis Rheum
  doi: 10.1002/art.30241
  contributor:
    fullname: Jeru
– volume: 280
  start-page: 39914
  year: 2005
  ident: 10.1002/art.30378-BIB7|cit7
  article-title: The CATERPILLER protein Monarch-1 is an antagonist of Toll-like receptor-, tumor necrosis factor α-, and Mycobacterium tuberculosis-induced pro-inflammatory signals
  publication-title: J Biol Chem
  doi: 10.1074/jbc.M502820200
  contributor:
    fullname: Williams
– volume: 105
  start-page: 1614
  year: 2008
  ident: 10.1002/art.30378-BIB4|cit4
  article-title: Mutations in NALP12 cause hereditary periodic fever syndromes
  publication-title: Proc Natl Acad Sci U S A
  doi: 10.1073/pnas.0708616105
  contributor:
    fullname: Jeru
– volume: 48
  start-page: 927
  year: 2003
  ident: 10.1002/art.30378-BIB11|cit11
  article-title: Anakinra, a recombinant human interleukin-1 receptor antagonist (r-metHuIL-1ra), in patients with rheumatoid arthritis: a large, international, multicenter, placebo-controlled trial
  publication-title: Arthritis Rheum
  doi: 10.1002/art.10870
  contributor:
    fullname: Fleischmann
– volume: 56
  start-page: 3138
  year: 2007
  ident: 10.1002/art.30378-BIB2|cit2
  article-title: Pattern of interleukin-1β secretion in response to lipopolysaccharide and ATP before and after interleukin-1 blockade in patients with CIAS1 mutations
  publication-title: Arthritis Rheum
  doi: 10.1002/art.22842
  contributor:
    fullname: Gattorno
– volume: 355
  start-page: 581
  year: 2006
  ident: 10.1002/art.30378-BIB1|cit1
  article-title: Neonatal-onset multisystem inflammatory disease responsive to interleukin-1β inhibition
  publication-title: N Engl J Med
  doi: 10.1056/NEJMoa055137
  contributor:
    fullname: Goldbach-Mansky
– volume: 277
  start-page: 29874
  year: 2002
  ident: 10.1002/art.30378-BIB6|cit6
  article-title: PYPAF7, a novel PYRIN-containing Apaf1-like protein that regulates activation of NF-κB and caspase-1-dependent cytokine processing
  publication-title: J Biol Chem
  doi: 10.1074/jbc.M203915200
  contributor:
    fullname: Wang
– volume: 185
  start-page: 4515
  year: 2010
  ident: 10.1002/art.30378-BIB8|cit8
  article-title: Cutting edge: NLRP12 controls dendritic and myeloid cell migration to affect contact hypersensitivity
  publication-title: J Immunol
  doi: 10.4049/jimmunol.1002227
  contributor:
    fullname: Arthur
SSID ssj0002353
ssj0000970605
Score 2.3782542
Snippet Objective A new class of autoinflammatory syndromes called NLRP12‐associated disorders (NLRP12AD) has been associated with mutations in NLRP12. Conflicting...
A new class of autoinflammatory syndromes called NLRP12-associated disorders (NLRP12AD) has been associated with mutations in NLRP12. Conflicting data on the...
OBJECTIVEA new class of autoinflammatory syndromes called NLRP12-associated disorders (NLRP12AD) has been associated with mutations in NLRP12. Conflicting data...
Objective: A new class of autoinflammatory syndromes called NLRP12-associated disorders (NLRP12AD) has been associated with mutations in NLRP12. Conflicting...
SourceID hal
proquest
crossref
pubmed
pascalfrancis
wiley
SourceType Open Access Repository
Aggregation Database
Index Database
Publisher
StartPage 2142
SubjectTerms Biological and medical sciences
Diseases of the osteoarticular system
Enzyme-Linked Immunosorbent Assay
Genetics
Hereditary Autoinflammatory Diseases - drug therapy
Hereditary Autoinflammatory Diseases - genetics
Hereditary Autoinflammatory Diseases - immunology
Humans
Immunology
Interleukin 1 Receptor Antagonist Protein - therapeutic use
Interleukin-1beta - metabolism
Intracellular Signaling Peptides and Proteins - genetics
Life Sciences
Male
Medical sciences
Prospective Studies
Signal Transduction
Title Role of interleukin‐1β in NLRP12‐associated autoinflammatory disorders and resistance to anti–interleukin‐1 therapy
URI https://onlinelibrary.wiley.com/doi/abs/10.1002%2Fart.30378
https://www.ncbi.nlm.nih.gov/pubmed/21480187
https://search.proquest.com/docview/874482632
https://inserm.hal.science/inserm-03894153
Volume 63
hasFullText 1
inHoldings 1
isFullTextHit
isPrint
link http://utb.summon.serialssolutions.com/2.0.0/link/0/eLvHCXMwnZ3datRAFIAPtRciiPXfVF0GUfAm252ZbDLBq6KWVdsii4VeCGEmM8GlbVK6iaB40UcQfBMfxIfok3hOJtlli4J4l2QyITNzzplz5ucbgKeFVEoLY0ORSxlGWsVhGgsXRsrGxP82pp1o39uPJwfR28Px4Rq86PfCeD7EYsCNNKO116Tg2sy3ltBQrNkh2t-ENvpymdByvlfTJTpKyI5ASSP_45T3VKGR2FrkXOmLrnyilZDXT_UcK6fwp1r8ye1c9WLbbmhnAz72BfCrT46GTW2G-ddLbMf_LOFNuNG5p2zby9MtWHPlbbi6103A34Fv0-rYsapghJk4O3bN0ay8OP_Of_3EJ2x_d_qeC7zXXaM7y3RTVyjFKHgn7YQ-sx3vc850aRlG--TBouixusIn9ezi_MeljzO_SezLXTjYef3h5STsDnAIc5lyMqSFcJzLcS4i55TWwuqRkVpaXRiBSVEe68KNYqKs5cKpOOK6SLm0yqUYW8l7sF5WpXsAzIh8bNFVlZFFM2ONxkAs0TKPUzNSuSgCeNI3ZXbqOR2ZJzKLDOsxa-sxgGfYyIt0ImtPtnezWYnafpIRahDdGfmZBzBYEYNFDhERLi4RAbBeLjJUR5pj0aWrmnlGpwkoYuAHcN_LyzIzJ1SPSgJ43rb63_8zw1imvdj891cfwjU_3E0riR_Ben3WuMfoL9VmgIrx5t2gVY_fB6EWow
link.rule.ids 230,314,780,784,885,1375,27924,27925,46294,46718
linkProvider Wiley-Blackwell
linkToHtml http://utb.summon.serialssolutions.com/2.0.0/link/0/eLvHCXMwnZ3ditQwFIAPuyuoIP6uWn_WIAredHaSdDopeLOoy6gzgwy7sDcSkibFYXfbZacVFC_2EQTfxAfxIfZJPKftzDCLgnjXNk1pknOSc3KSLwDPMqmUEdaFIpUyjIyKwyQWPoyUi4n_bW0daB-N48F-9O6gd7AGL-d7YRo-xGLCjTSj7q9JwWlCentJDcWq7WAH3FfrcAnVndOCrteTJTxKyJZBSXP_vYTPuUJdsb3IujIarX-itZDXTswMqydrzrX4k-G5asfWA9HuDfg4L0Kz_uSwU5W2k369QHf83zLehOuthcp2GpG6BWs-vw2XR20M_g58mxRHnhUZI9LE6ZGvDqf5-dl3_usnPmHj4eQDF3hv2nb3jpmqLFCQUfaO65g-cy3yc8ZM7hg6_GTEovSxssAn5fT87MeFj7Nmn9iXTdjffbP3ahC2ZziEqUw49aWZ8JzLXioi75UxwpmulUY6k1mBSVEam8x3YwKtpcKrOOImS7h0yifoXsm7sJEXub8PzIq059BalZHDnsZZg75Y38g0TmxXpSIL4Om8LfVJg-rQDZRZaKxHXddjAM-xlRfpBNce7Az1NEeFP9ZEG0SLRn7mAWytyMEih4iIGNcXAbC5YGjUSAqzmNwX1UzTgQKKMPgB3GsEZpmZE61H9QN4UTf73_9ToztTXzz491efwJXB3mioh2_H7x_C1Wb2mxYWP4KN8rTyj9F8Ku1WrSW_AcXDGcs
linkToPdf http://utb.summon.serialssolutions.com/2.0.0/link/0/eLvHCXMwnZ3dahQxFIAPbYUiSP23408NouDNbDfJ7GwGr4p1WXW7lMVCL4SQv8Gl7czSnREUL_oIgm_ig_gQfRJP5meXLQri3cxkMkySc5JzcpIvAM9TLoRi2obMcB5GSsRhEjMXRsLGnv-tdRVoPxjHw6Po3XHveA1etXthaj7EYsLNa0bVX3sFn9l0dwkNxZrtYP_bF-twLYpZ4sH5-5MlO4rxBkHpp_57CW2xQl22u8i6Mhitf_JLIW_M1BxrJ62PtfiT3blqxlbj0OAmfGxLUC8_OemUhe6Yr1fgjv9ZxFuw1dinZK8WqNuw5rI7sHnQRODvwrdJfupInhLPmTg_deXJNLu8-E5__cQnZDyaHFKG96ppdWeJKoscxRgl76yK6BPbAD_nRGWWoLvvTViUPVLk-KSYXl78uPJxUu8S-3IPjgZvPrwehs0JDqHhCfU9acocpbxnWOScUIpZ1dVccatSzTApMrFKXTf2mDXDnIgjqtKEcitcgs4Vvw8bWZ65bSCamZ5FW5VHFvsZqxV6Yn3FTZzorjAsDeBZ25RyVoM6ZI1kZhLrUVb1GMALbORFukdrD_dGcpqhup9JzxpEe4Z_pgHsrIjBIgeLPC-uzwIgrVxI1EcfZFGZy8u59McJCA_BD-BBLS_LzNSzekQ_gJdVq__9PyU6M9XFw39_9SlsHu4P5Ojt-P0juF5PfftVxY9hozgv3RO0nQq9U-nIb3oSGHo
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=Role+of+interleukin-1%CE%B2+in+NLRP12-associated+autoinflammatory+disorders+and+resistance+to+anti-interleukin-1+therapy&rft.jtitle=Arthritis+and+rheumatism&rft.au=J%C3%A9ru%2C+Isabelle&rft.au=Hentgen%2C+V%C3%A9ronique&rft.au=Normand%2C+Sylvain&rft.au=Duquesnoy%2C+Philippe&rft.date=2011-07-01&rft.eissn=1529-0131&rft.volume=63&rft.issue=7&rft.spage=2142&rft_id=info:doi/10.1002%2Fart.30378&rft_id=info%3Apmid%2F21480187&rft.externalDocID=21480187
thumbnail_l http://covers-cdn.summon.serialssolutions.com/index.aspx?isbn=/lc.gif&issn=0004-3591&client=summon
thumbnail_m http://covers-cdn.summon.serialssolutions.com/index.aspx?isbn=/mc.gif&issn=0004-3591&client=summon
thumbnail_s http://covers-cdn.summon.serialssolutions.com/index.aspx?isbn=/sc.gif&issn=0004-3591&client=summon