PMID- 23452551
OWN - NLM
STAT- MEDLINE
DCOM- 20150603
LR  - 20211021
IS  - 1478-6362 (Electronic)
IS  - 1478-6354 (Print)
IS  - 1478-6354 (Linking)
VI  - 15
IP  - 2
DP  - 2013 Mar 1
TI  - The severity of experimental arthritis is independent of IL-36 receptor 
      signaling.
PG  - R38
LID - 10.1186/ar4192 [doi]
AB  - INTRODUCTION: Interleukin (IL)-36 refers to three related IL-1 family cytokines, 
      IL-36alpha, IL-36beta, and IL-36gamma, that bind to the IL-36 receptor (IL-36R). IL-36 
      exerts proinflammatory effects in skin and lung and stimulates T cell responses. 
      In the present study, we examined the expression and function of IL-36R and its 
      ligands in experimental arthritis. METHODS: Collagen-induced arthritis (CIA), 
      antigen-induced arthritis (AIA), and K/BxN serum transfer-induced arthritis were 
      induced according to standard protocols. Messenger RNA levels for IL-36R and its 
      ligands in the joints of mice with CIA were determined by RT-qPCR. Mice with CIA 
      were injected with a blocking monoclonal anti-IL-36R, a blocking anti-IL-1RI, or 
      their isotype-matched control antibodies at the time of arthritis onset. 
      Anti-IL-36R or control antibodies were also injected at the time of AIA 
      induction. Finally, IL-36R-deficient mice were examined in AIA and serum 
      transfer-induced arthritis. The development and severity of arthritis were 
      assessed by clinical and histological scoring. RESULTS: IL-36R, IL-36Ra and 
      IL-36gamma mRNA were detected in the joints of mice with CIA, but their levels did 
      not correlate with arthritis severity. As opposed to anti-IL-1RI antibody 
      treatment, the injection of an anti-IL-36R antibody was devoid of effect on the 
      development and severity of CIA. The severity of joint inflammation and 
      structural damage in AIA was also unaltered by anti-IL-36R antibody treatment. 
      Finally, the severity of AIA and K/BxN serum transfer-induced arthritis was 
      similar in IL-36R-deficient and wild-type mice. CONCLUSIONS: The development and 
      severity of experimental arthritis are independent of IL-36R signaling.
FAU - Lamacchia, Celine
AU  - Lamacchia C
FAU - Palmer, Gaby
AU  - Palmer G
FAU - Rodriguez, Emiliana
AU  - Rodriguez E
FAU - Martin, Praxedis
AU  - Martin P
FAU - Vigne, Solenne
AU  - Vigne S
FAU - Seemayer, Christian A
AU  - Seemayer CA
FAU - Talabot-Ayer, Dominique
AU  - Talabot-Ayer D
FAU - Towne, Jennifer E
AU  - Towne JE
FAU - Gabay, Cem
AU  - Gabay C
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20130301
PL  - England
TA  - Arthritis Res Ther
JT  - Arthritis research & therapy
JID - 101154438
RN  - 0 (Receptors, Interleukin-1)
RN  - 0 (interleukin-36 receptor, mouse)
SB  - IM
MH  - Animals
MH  - Arthritis, Experimental/*immunology/metabolism/*pathology
MH  - Mice
MH  - Mice, Inbred C57BL
MH  - Mice, Inbred DBA
MH  - Real-Time Polymerase Chain Reaction
MH  - Receptors, Interleukin-1/*immunology/metabolism
MH  - *Signal Transduction/immunology
PMC - PMC3672771
EDAT- 2013/03/05 06:00
MHDA- 2015/06/04 06:00
PMCR- 2013/03/01
CRDT- 2013/03/05 06:00
PHST- 2012/11/04 00:00 [received]
PHST- 2013/03/01 00:00 [accepted]
PHST- 2013/03/05 06:00 [entrez]
PHST- 2013/03/05 06:00 [pubmed]
PHST- 2015/06/04 06:00 [medline]
PHST- 2013/03/01 00:00 [pmc-release]
AID - ar4192 [pii]
AID - 10.1186/ar4192 [doi]
PST - epublish
SO  - Arthritis Res Ther. 2013 Mar 1;15(2):R38. doi: 10.1186/ar4192.