| First Author | Li X | Year | 2017 |
| Journal | Clin Immunol | Volume | 180 |
| Pages | 63-68 | PubMed ID | 28396236 |
| Mgi Jnum | J:271874 | Mgi Id | MGI:6282252 |
| Doi | 10.1016/j.clim.2017.03.015 | Citation | Li X, et al. (2017) Skin inflammation induced by lupus serum was inhibited in IL-1R deficient mice. Clin Immunol 180:63-68 |
| abstractText | Skin inflammation induced by lupus serum is a useful tool to investigate the pathogenesis of lupus skin injury. IL-1 is a proinflammatory cytokine, and its role in lupus skin lesion is still unclear. We determined the role of IL-1 in lupus skin injury by using gene deficient mice. We found that 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 FcgammaRI (CD64), FcgammaRII (CD32) and MHC class II (CD74) induced by lupus serum. IL-1R deficiency reduced the lipid raft clustering, and decreased expression of MCP-1 and TNFalpha in monocytes. Keratinocyte proliferation induced by lupus serum was significantly decreased in TNFalpha 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. |
