Translational autoimmunity in pemphigus and the role of novel Bruton tyrosine kinase inhibitors

Bruton tyrosine kinase (BTK) is involved in a multifarious inflammatory and autoimmune process. As a result, BTK has emerged as a promising novel remedial target for amalgamated autoimmune diseases. Medicament corporations have recently devoted considerable attention to the evolution of BTK inhibitors. Pemphigus is an uncommon and often fatal autoimmune illness. Blisters and erosions on cutaneous surfaces and mucous membranes are crippling symptoms of pemphigus vulgaris, which are caused by immunoglobulin G autoantibodies binding to keratinocyte proteins, resulting in keratinocyte adhesion defects. Although systemic corticosteroids and adjuvant medications are used to treat pemphigus, some patients are resistant to these. BTK inhibitors inhibit B-cell signaling, which is clinically useful in treating pemphigus. Assorted clinical trials are underway to assess the safety, tolerability, and pharmacokinetics of distinct BTK inhibitors, including PRN473 and remibrutinib. The current review evaluates translational autoimmunity in pemphigus and discusses BTK inhibitors in the treatment of pemphigus.