Abstract
Cutaneous Lupus Erythematosus (CLE) is a clinically diverse group of autoimmune skin diseases with shared histological features of interface dermatitis and autoantibodies deposited at the dermal–epidermal junction. Various genetic and environmental triggers of CLE promote infiltration of T cells, B cells, neutrophils, antigen presenting cells, and NK cells into lesional skin. In this mini-review, we will discuss the clinical features of CLE, insights into CLE immunopathogenesis, and novel treatment approaches.
Highlights
Cutaneous Lupus Erythematosus (CLE) is an autoimmune disease primarily affecting skin and mucosal tissue
Up to 80% of systemic lupus erythematosus (SLE) patients experience malar rash, which typically flares with UV exposure but does not leave any scar or dyspigmentation
In the SLE studies, blood NK numbers decrease with increased lupus disease activity and/or exhibit defects in traditional killing functions [129,130,131]; though rare populations are often expanded and secrete higher levels of IFNγ compared to healthy controls [132,133,134,135]
Summary
Cutaneous Lupus Erythematosus (CLE) is an autoimmune disease primarily affecting skin and mucosal tissue. In the SLE studies, blood NK numbers decrease with increased lupus disease activity and/or exhibit defects in traditional killing functions [129,130,131]; though rare populations are often expanded and secrete higher levels of IFNγ compared to healthy controls [132,133,134,135] Given their roles in sensing cellular stress [136], clearing tumors [137, 138], and keratinocyte-derived tumors in particular [139], it is likely that NK cells are able to kill stressed keratinocytes following UV or drug injury to promote CLE lesions. Overexpression of Vgll in male mice makes skin appear more “female-like” and promotes both skin and systemic autoimmune attack [168]
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