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The Journal of Immunology, 2002, 169: 5851-5859.
Copyright © 2002 by The American Association of Immunologists

Development of Inflammation in Proteoglycan-Induced Arthritis Is Dependent on Fc{gamma}R Regulation of the Cytokine/Chemokine Environment1

Charles D. Kaplan2,*, Shannon K. O’Neill*, Tamas Koreny{dagger}, Matyas Czipri{dagger} and Alison Finnegan*,{ddagger}

Departments of * Immunology/Microbiology, {dagger} Orthopedic Surgery, and {ddagger} Medicine, Section of Rheumatology, Rush-Presbyterian-St. Luke’s Medical Center, Chicago, IL 60612

Fc{gamma}Rs are specialized cell surface receptors that coordinately regulate immune responses. Although Fc{gamma}R expression is a prerequisite for the development of several immune complex-mediated diseases, the mechanism responsible for Fc{gamma}R-dependent regulation in autoimmunity remains unclear. Therefore, we assessed Fc{gamma}R-dependent regulation of inflammation in proteoglycan-induced arthritis (PGIA) using Fc{gamma}R-/- mice. Fc{gamma}RIIb-/- mice developed arthritis at an earlier time point and with a greater severity than wild-type (WT) mice. In {gamma}-chain-/- (Fc{gamma}RI-/- and Fc{gamma}RIII-/-) mice, no clinical or histological evidence of inflammation was observed. Exacerbation of arthritis in Fc{gamma}RIIb-/- mice correlated with enhanced PG-specific Ab production, but did not significantly affect PG-specific T cell priming. In {gamma}-chain-/- mice, the absence of arthritis did not correlate with serum Ab responses, as PG-specific Ab production was normal. Although PG-specific T cell proliferation was diminished, spleen cells from {gamma}-chain-/- mice successfully adoptively transferred arthritis into SCID mice. Our studies indicated that the mechanism responsible for Fc{gamma}R regulation of PGIA development was at the level of inflammatory cytokine and {beta}-chemokine expression within the joint. Fc{gamma}RIIb regulated the development of PGIA by controlling the initiation of cytokine and chemokine expression within the joint before the onset of arthritis, whereas the expression of Fc{gamma}RI and or Fc{gamma}RIII controlled cytokine and chemokine expression late in the development of PGIA during the onset of disease. These results suggest that Fc{gamma}Rs are critical for the development of inflammation during PGIA, possibly by maintaining or enhancing inflammatory cytokine and {beta}-chemokine production.




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