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*
Department of Immunology and
Centre for Rheumatic Diseases, University of Glasgow, Glasgow, United Kingdom
IL-18 expression has recently been detected in rheumatoid arthritis
(RA) synovial membrane. We investigated the mechanisms by which
IL-18-induced collagen-induced arthritis in DBA/1 mice primed
intradermally with type II bovine collagen in IFA and boosted i.p. 21
days later with CII in saline. Mice were injected i.p. with rIL-12,
rIL-18, or both (100 ng) during days -1 to 4 and again on days 20–24.
Control mice received PBS. Mice treated with IL-12 or IL-18 alone
developed significantly higher incidence and more severe disease
compared with controls. These were elevated further by combination
treatment with IL-12 and IL-18. The cytokine treatments led to markedly
enhanced synovial hyperplasia, cellular infiltration, and cartilage
erosion compared with controls. Cytokine-treated mice produced
significantly more IFN-
, TNF-
, and IL-6 than the controls.
Interestingly, IL-18-treated mice produced more TNF- and IL-6, but
less IFN-, compared with mice treated with IL-12. Furthermore,
splenic macrophages from DBA/1 mice cultured in vitro with IL-18, but
not IL-12, produced substantial amounts of TNF-. Mice treated with
IL-18 or IL-18 plus IL-12 produced markedly more IgG1 and IgG2a
anti-collagen Ab compared with controls, whereas IL-12 treatment
only led to an enhanced IgG2a response. Together these results
demonstrate that IL-18 can promote collagen-induced inflammatory
arthritis through mechanisms that may be distinct from those induced by
IL-12.
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