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Keratinocyte cellular membrane and cytoplasmic components refer to a broad assembly of structural and signaling proteins within the primary cells of the epidermis that maintain skin integrity. These components include critical adhesion molecules such as desmogleins (Dsg1 and Dsg3) and desmocollins, which are located on the cell membrane, as well as various intracellular proteins like plakoglobin and desmoplakin found in the cytoplasm [1][2]. In autoimmune bullous diseases like Pemphigus vulgaris and Pemphigus foliaceus, these components become the targets of IgG autoantibodies, leading to the loss of cell-to-cell adhesion known as acantholysis [1][3]. While this term does not describe a single therapeutic target, it is frequently used in diagnostic immunology to describe the substrate for indirect immunofluorescence tests used to identify circulating antiepidermal antibodies [3]. Therapeutic management of conditions involving these targets does not involve direct binding to the keratinocyte components but rather focuses on systemic immunosuppression using agents like Rituximab or corticosteroids to halt the autoimmune attack [4][5]. Consequently, this entry represents a complex of antigens rather than a discrete molecular target for drug development.
Therapeutic intervention typically involves systemic immunosuppression or B-cell depletion to reduce the production of autoantibodies directed against these cellular components, rather than direct binding to the components themselves [4][5].
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