In:
The Journal of Immunology, The American Association of Immunologists, Vol. 198, No. 1_Supplement ( 2017-05-01), p. 55.7-55.7
Abstract:
Skin lesion is the second common clinical manifestations of systemic lupus erythematosus (SLE), but its pathogenesis is not clear. IL-1 is a proinflammatory cytokine, and its role in SLE skin lesion is still unclear. We used IL-1R deficient mice and other gene deficient mice to study the role of IL-1 in the lupus serum -induced skin inflammation. We found that the severity of skin inflammation induced by lupus serum was significantly reduced in IL-1R deficient mice and caspase-1 deficient mice. IL-1R deficiency did not affect the expression of FcγRI (CD64), FcγRII (CD32) and MHC class II (CD74) induced by lupus serum. IL-1R deficiency also reduced the lipid raft clustering, and decreased expression of MCP-1 and TNFa in monocytes. Skin inflammation and keratinocyte proliferation were significantly decreased in TNFa deficient mice. Our findings indicate that IL-1 plays an important role in skin lesions of SLE. This study suggests that IL-1 is a therapeutic target in skin lesions of SLE.
Type of Medium:
Online Resource
ISSN:
0022-1767
,
1550-6606
DOI:
10.4049/jimmunol.198.Supp.55.7
Language:
English
Publisher:
The American Association of Immunologists
Publication Date:
2017
detail.hit.zdb_id:
1475085-5
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