The role of T cells in pemphigus vulgaris and bullous pemphigoid

Pemphigus vulgaris (PV) and bullous pemphigoid (BP) are autoantibody-mediated diseases clinically characterized by blisters and erosions of skin and/or mucous membranes. Immune imbalance and antibody generation are the key pathologies of autoimmune bullous diseases. Recently, a large number of studies have shown that T cell subsets, which are critical players in autoimmunity, exhibit a range of abnormalities and drive immunopathogenesis and skin inflammation in PV and BP. T helper (Th)1 cells mediate pro-inflammatory or immune responses through IFN-gamma and Th2-derived cytokines, such as IL-4, can promote B cell proliferation, antibody production and immunoglobulin class-switching. Th17 cells promote inflammatory response and skin damage, while regulatory T cells suppress autoreactive CD4(+) T cell activation and help control inflammation. T follicular helper cells cross-talk with B cells and facilitate autoantibody production. In this review, we discuss the immune features of PV and BP, with a focus on the aberrations in T cell subsets, such as Th1 cells, Th2 cells, Th17 cells, regulatory T cells, T follicular helper cells, CD8(+) T cells, gamma delta T cells and resident memory T cells in the pathogenesis of PV and BP. Improved understanding of biological and immunological functions of T cell subsets in patients with autoimmune skin disorders will offer unique opportunities for the recognition of treatment targets for these complex diseases.