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- Title
CD11b-deficient mice exhibit an increased severity in the late phase of antibody transfer-induced experimental epidermolysis bullosa acquisita.
- Authors
Deng, Fengyuan; Chen, Yan; Zheng, Junfeng; Huang, Qiaoniang; Cao, Xuetao; Zillikens, Detlef; Petersen, Frank; Yu, Xinhua
- Abstract
CD11b, the α-chain of β2 integrin Mac-1, is involved in many activation processes of phagocytes. Depending on the respective autoimmune disorder, CD11b has been shown to exert pro-inflammatory functions or be dispensable in their pathogenesis. Here, we investigated the role of CD11b in the pathogenesis of experimental epidermolysis bullosa acquisita ( EBA), an autoimmune skin blistering disease mediated by autoantibodies to type VII collagen. Unexpectedly, in an antibody transfer-induced model of EBA, CD11b-deficient mice developed more severe disease symptoms than wild-type mice in the late phase of the disease. Furthermore, as compared to wild-type controls, CD11b-deficient mice expressed increased levels of circulating IFN-γ and IL-4. Taken together, for the first time, our results suggest an anti-inflammatory role for CD11b in experimental autoimmune diseases.
- Subjects
AUTOIMMUNE diseases; IMMUNOLOGIC diseases; AUTOANTIBODIES; CRYOGLOBULINS; ANTINUCLEAR factors
- Publication
Experimental Dermatology, 2017, Vol 26, Issue 12, p1175
- ISSN
0906-6705
- Publication type
Article
- DOI
10.1111/exd.13434