Abstract
Cutaneous lupus erythematosus (CLE) is an autoimmune skin disease characterized by high IFN expression. Recent advances have challenged the Th1-Th2 paradigm in CLE, as there are reports of expression of both Th1 and Th2 cytokines in lesional skin. We assessed the role of T cell skewing in the initiation of skin disease using a lupus-prone mouse model of CLE that depends on recognizing cognate antigen by infiltrating T cells in an immune environment perturbed by a TLR7-driven type I IFN response.
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