| Article ID | Journal | Published Year | Pages | File Type |
|---|---|---|---|---|
| 3256804 | Clinical Immunology | 2016 | 8 Pages |
•Systemic lupus erythematosus (SLE) is characterized by high levels of autoantibodies in serum and multiorgan damage.•IgG is deposited in the skin of patients with SLE.•Lupus serum can induce skin inflammation.•IgG in lupus serum directly induced skin inflammation.•Lupus IgG and CpG DNA synergistically induced skin inflammation.
We recently developed a model of lupus serum-induced skin inflammation, which was used to study the pathogenesis of skin injury in systemic lupus erythematosus (SLE). We further characterized the features of lupus serum-induced skin inflammation. This skin inflammation was evident within 3 h and lasted for at least two weeks. The skin inflammation was characterized by an influx of monocytic, CD11b + cells and by a scarcity of T and B lymphocytes. Depletion of IgG from the serum abrogated the skin inflammatory response. The skin inflammation was related to lupus patients' skin history but not to SLE disease activity and type of autoantibody. The expression of TNFR1, NF-kB and MCP-1 was increased locally in skin lesions. The TLR9 ligand and lupus serum act synergistically to trigger skin inflammation. These findings suggest that this novel model is valuable for the study of the pathogenesis and therapy of skin injury in SLE.
