Background and aims Systemic lupus erythematosus (SLE) is a seriously chronic autoimmune disease, which is characterised by a large number of autoantibodies and multiple organ damage. Skin lesion is one of the common clinical manifestations of lupus erythematosus, but its pathogenesis is not clear. IL-1 is a proinflammatory cytokine, the aim in this study is to investigate the role of IL-1 in the skin injury in SLE.
Methods We used IL-1 receptor deficient mice and other gene deficient mice to study the role of IL-1 in the lupus serum IgG -induced skin inflammation.
Results We found that the severity of skin lesion in IL-1 receptor deficient mice and caspase-1 deficient mice was reduced compared with that in wild type mice. IL-1 receptor deficiency suppressed the expression of FcγRI (CD64) and MHC class II (CD74), and increased the level of FcγRII (CD32) induced by lupus serum. IL-1 receptor deficiency also suppressed the lipid raft clustering and IFN-γ in T cells, and reduced IgG internalisation and presentation in macrophage, and decreased expression of MCP-1 and TNFa in monocytes. In addition, TNFa could promote the proliferation of kerationocytes.
Conclusions Our findings indicate that IL-1 plays an important role in skin lesions of lupus erythematosus. This study suggests IL-1 is a therapeutic target in skin lesions of systemic lupus erythematosus.
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