First Author | Nandakumar KS | Year | 2006 |
Journal | Eur J Immunol | Volume | 36 |
Issue | 6 | Pages | 1608-18 |
PubMed ID | 16688680 | Mgi Jnum | J:115066 |
Mgi Id | MGI:3690605 | Doi | 10.1002/eji.200535633 |
Citation | Nandakumar KS, et al. (2006) Arthritis induced with cartilage-specific antibodiesis IL-4-dependent. Eur J Immunol 36(6):1608-18 |
abstractText | It is widely believed that IL-4 exerts its influence by profiling the immune response during priming and expansion of immune cells, and thereby modulates the outcome of chronic inflammation. In the present investigation, collagen antibody-induced arthritis (CAIA) was used to delineate the role of IL-4 in a T cell-independent inflammatory phase. Mice predisposed to Th2 cytokines (BALB/c and STAT4-deficient mice) developed a more severe arthritis than mice biased towards Th1 cytokines (C57BL/6 and STAT6-deficient mice). Reduced incidence of CAIA was observed in IL-4-deficient mice compared to control littermates. Infiltrating cells in the paws of IL-4-sufficient mice had increased osteoclast activity and tumor necrosis factor (TNF)-alpha and interleukin (IL)-1beta secretion. Massive infiltration of granulocytes and joint and cartilage damage were present in arthritic paws. Depletion of IL-4 suppressed CAIA, which was abrogated by IFN-gamma neutralization. IL-1R- and IL-1RTNFR-deficient mice were completely resistant to CAIA. Thus, IL-4 promotes an antibody-mediated and TNF-alpha/IL-1beta-dependent inflammation in vivo. |