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*
Department of Immunology and Bacteriology and
Centre for Rheumatic Diseases, University of Glasgow, Glasgow, G11 6NT, United Kingdom
We have recently reported the presence and a potential
proinflammatory role of IL-18 in the synovium of patients with
rheumatoid arthritis. To obtain direct evidence that IL-18 plays an
influential role in articular inflammation, we investigated the
development of collagen-induced arthritis in a strain of mice lacking
IL-18 (IL-18-/-) of DBA/1 background.
IL-18-/- mice developed markedly reduced incidence of
arthritis compared with heterozygous or wild-type mice. Of the
IL-18-/- mice that developed arthritis, the severity of
the disease was significantly reduced compared with the intact mice.
This was accompanied by reduced articular inflammation and destruction
evident on histology. IL-18-/- mice also had
significantly reduced Ag-specific proliferation and proinflammatory
cytokine (IFN-
, TNF-
, IL-6, and IL-12) production by spleen and
lymph node cells in response to bovine type II collagen (CII) in vitro
compared with wild-type mice, paralleled in vivo by a significant
reduction in serum anti-CII IgG2a Ab level. Treatment with rIL-18
completely reversed the disease of the IL-18-/- mice to
that of the wild-type mice. These data directly demonstrate a pivotal
role of IL-18 in the development of inflammatory arthritis and suggest
that antagonists to IL-18 may have therapeutic potential in rheumatic
diseases.
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