Document Detail


Interleukin-22 reduces the severity of collagen-induced arthritis in association with increased levels of interleukin-10.
MedLine Citation:
PMID:  23334981     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
OBJECTIVE: The mechanism of action of interleukin- 22 (IL-22) in inflammatory arthritis remains unknown. IL-22-deficient mice exhibit an intact humoral and cellular immune response to collagen and yet have a reduced incidence of collagen-induced arthritis (CIA). Further, administration of anti-IL-22 does not reduce the severity of clinical arthritis but rather improves only certain aspects of joint inflammation as assessed histologically. This study was undertaken to investigate the mechanism of action and role of systemic IL-22 in modulating target organ inflammation.
METHODS: CIA was induced in DBA mice by immunization with collagen and Freund's complete adjuvant. Expression of IL-22 and its receptor (IL-22R) in lymphoid organ and target tissues was determined during various phases of arthritis. The effector functions of IL-22 on induction/regulation of various cytokines in in vitro restimulation cultures were analyzed by enzyme-linked immunosorbent assay (ELISA). Recombinant IL-22 with or without anti-IL-10 antibody was administered to mice following immunization with collagen and prior to the onset of arthritis, and the severity of arthritis was evaluated by clinical scoring and histopathologic assessment. Anticollagen antibodies in mouse sera were analyzed by ELISA.
RESULTS: IL-22 and IL-22R were up-regulated in lymphoid organs and joints during the course of arthritis. IL-22 augmented IL-10, IL-17, and IL-6 in lymphoid tissues in vitro. Administration of recombinant IL-22 was associated with an increase in IL-10 levels in vivo and a significant reduction in the progression of arthritis severity. Anti-IL-10 antibody treatment was associated with the abrogation of this protective effect of IL-22.
CONCLUSION: Our data demonstrate, for the first time, that IL-22 has a protective role in inflammatory arthritis.
Authors:
Sujata Sarkar; Xiaoqun Zhou; Shivali Justa; Swaroopa Rani Bommireddy
Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  Arthritis and rheumatism     Volume:  65     ISSN:  1529-0131     ISO Abbreviation:  Arthritis Rheum.     Publication Date:  2013 Apr 
Date Detail:
Created Date:  2013-04-04     Completed Date:  2013-05-22     Revised Date:  2014-04-02    
Medline Journal Info:
Nlm Unique ID:  0370605     Medline TA:  Arthritis Rheum     Country:  United States    
Other Details:
Languages:  eng     Pagination:  960-71     Citation Subset:  AIM; IM    
Copyright Information:
Copyright © 2013 by the American College of Rheumatology.
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MeSH Terms
Descriptor/Qualifier:
Animals
Arthritis, Experimental / immunology,  metabolism*
Cytokines / metabolism
Disease Models, Animal
Gene Expression Profiling
Interleukin-10 / metabolism*,  secretion
Interleukin-17 / metabolism
Interleukin-6 / metabolism
Interleukins / genetics,  metabolism*
Joints / metabolism
Lymph Nodes / metabolism
Mice
Mice, Inbred DBA
RNA, Messenger / analysis*
Receptors, Interleukin / genetics,  metabolism*
Spleen / cytology,  metabolism,  secretion
Grant Support
ID/Acronym/Agency:
AR-054323/AR/NIAMS NIH HHS; K08 AR054323/AR/NIAMS NIH HHS
Chemical
Reg. No./Substance:
0/Cytokines; 0/IL10 protein, mouse; 0/Interleukin-17; 0/Interleukin-6; 0/Interleukins; 0/RNA, Messenger; 0/Receptors, Interleukin; 0/interleukin-22; 0/interleukin-22 receptor; 130068-27-8/Interleukin-10
Comments/Corrections

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