Mechanisms of skin autoimmunity: Cellular and soluble immune components of the skin

Autoimmune diseases are driven by either T cells or antibodies reacting specifically to 1 or more self-antigens. Although a number of self-antigens associated with skin diseases have been identified, the causative antigen(s) remains unknown in the great majority of skin diseases suspected to be autoimmune driven. Model diseases such as pemphigus, dermatitis herpetiformis, and more recently psoriasis have added greatly to our understanding of skin autoimmunity. Depending on the dominant T- or B-cell phenotype, skin autoimmune diseases usually follow 1 of 6 immune response patterns: lichenoid, eczematous, bullous, psoriatic, fibrogenic, or granulomatous. Usually, skin autoimmunity develops as a consequence of several events—an altered microbiome, inherited dysfunctional immunity, antigens activating innate immunity, epigenetic modifications, sex predisposition, and impact of antigens either as neoantigen or through molecular mimicry. This review summarizes currently known antigens of skin autoimmune diseases and discusses mechanisms of skin autoimmunity.