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*
Alexion Pharmaceuticals, Inc., New Haven, CT 06511; and
Department of Pathology, Yale University School of Medicine, New Haven, CT 06520
Collagen-induced arthritis (CIA) represents an animal model of
autoimmune polyarthritis with significant similarities to human
rheumatoid arthritis that can be induced upon immunization with native
type II collagen. As in rheumatoid arthritis, both cellular and humoral
immune mechanisms contribute to disease pathogenesis. Genotypic studies
have identified at least six genetic loci contributing to arthritis
susceptibility, including the class II MHC. We have examined the
mechanism of Ab-mediated inflammation in CIA joints, specifically the
role of complement activation, by deriving a line of mice from the
highly CIA-susceptible DBA/1LacJ strain that are congenic for
deficiency of the C5 complement component. We show that such
C5-deficient DBA/1LacJ animals mount normal cellular and humoral immune
responses to native type II collagen, with the activation of
collagen-specific TNF-
-producing T cells in the periphery and
substantial intra-articular deposition of complement-fixing IgG Abs.
Nevertheless, these C5-deficient mice are highly resistant to the
induction of CIA. These data provide evidence for an important role of
complement in Ab-triggered inflammation and in the pathogenesis of
autoimmune arthritis.
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