Abstract

Pemphigus vulgaris (PV) is characterized by loss of immune tolerance against the desmosomal components Desmoglein (Dsg) 1 and 3 resulting in pathogenic IgG autoantibodies which cause loss of epithelial cell adhesion in skin and mucous membranes. Autoreactive CD4+ T cells have been shown to be key drivers of PV as they help B cells in maturation and anti-Dsg3 IgG production. Their detection and further characterization is thus important for identification of potential checkpoints and development of novel therapies, although being quite challenging due to their low frequency in peripheral blood.

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