Arthritis critically dependent on innate immune system players.

By H. Ji, K. Ohmura, Umar Mahmood, David M. Lee, F. Hofhuis, S. Boackle, Kazue Takahashi, V. Holers, M. Walport, C. Gerard and 9 more. Immunity, 2002

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Evolving concepts of rheumatoid arthritis (2003, background): “Elegant molecular studies using knockout mice demonstrate an absolute requirement for FcγR (especially FcγRIII) and components of the alternative complement cascade (for example, Factor B) as well as complement proteins C3 and C”
The Role of the Anaphylatoxins in Health and Disease (2009, positive): “Indeed, contribution of both FcγRs and C5aR has been shown in models of IC-alveolitis and peritonitis (Baumann et al., 2000;Heller et al., 1999a), rheumatoid arthritis (Ji et al., 2002), autoimmune vitiligo (Trcka et al., 2002), and autoimmune hemolytic anemia (AIHA) (Kumar et al., 2006).”
Fcγ receptors as regulators of immune responses (2008, background): “In model systems in which the IgG1 subclass is exclusively responsible for the phenotype, as for example in the K/BxN serum transfer arthritis model or in antibody-mediated tumour-cell, platelet or red-blood-cell depletion studies, animals deficient in FcγRIII showed abrogated antibody activit”
Complement C5a receptors and neutrophils mediate fetal injury in the antiphospholipid syndrome. (2003, background): “The linkage of alternative pathway activation with neutrophil infiltration may also account for the resistance of mice deficient in fB, C3, C5/C5aR, or neutrophils to joint damage after treatment with arthritogenic Ab’s, a phenotype that parallels our model (38, 45, 46, 54, 55).”