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Receptor
Departments of
*
Orthopaedic Surgery, and
Microbiology and Immunology, Hamamatsu University School of Medicine, Hamamatsu, Japan; and
Department of Pathology, Tokyo Metropolitan Geriatric Hospital, Tokyo, Japan
Collagen-induced arthritis (CIA) is an arthritic model that was
developed after immunization with type II collagen (CII). Apparently,
contradictory results have been reported regarding the role of IFN-
in the development of CIA. Therefore, we employed IFN-R-deficient
mice to study the role of IFN-. To introduce the CIA susceptibility
gene (H-2q), IFN-R-deficient
(H-2b/b/IFN-R-/-) mice were mated with
DBA/1 (H-2q/q/IFN-R+/+) mice; next, the
F1 mice were interbred to yield F2 offspring
bearing different combinations of H-2 (H-2q/q,
H-2q/b, and H-2b/b) and IFN-R
(IFN-R+/+, IFN-R+/-, and
IFN-R-/-) genes. Although the H-2q allele
appeared to confer susceptibility to CIA, mice that were homozygous for
the IFN-R mutation showed a substantially decreased incidence and
severity of CIA. The CII-specific IgG levels of serum samples, which
are known to be involved in the development of CIA, were remarkably
reduced in IFN-R-/- mice. Furthermore, the
anti-CII IgG2a levels controlled by IFN-R were significantly
reduced in IFN-R-/- F2 mice compared with
those seen in IFN-R+/+ and IFN-R+/-
mice, although the levels of all IgG subclass Abs examined were lower
in IFN-R-/- mice than in IFN-R+/+ mice.
No clear evidence of the imbalance of Th1/Th2 cytokines was observed in
CII-immunized, IFN-R-deficient mice. Taken together, these results
suggest that IFN- exacerbates CIA by affecting, at least, levels of
CII-specific IgG Ab rather than the imbalance of Th1/Th2
cells.
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