Plasma exosomal regulates mitochondria-dependent keratinocyte apoptosis by targeting XIAP in severe drug-induced skin reactions.

Stevens-Johnson syndrome (SJS) and toxic epidermal necrolysis (TEN) are severe drug-induced cutaneous reactions characterized by keratinocyte apoptosis. Exosomes are nanometer-sized membranous vesicles in body fluids. They contain functional proteins, mRNAs, and miRNAs, which induce immune dysfunction and influence disease progression.

Small interfering RNA targeting of keratin 17 reduces inflammation in imiquimod-induced psoriasis-like dermatitis.

Background: Psoriasis is a common chronic inflammatory skin disease with 2% to 3% prevalence worldwide and a heavy social-psychological burden for patients and their families. As the exact pathogenesis of psoriasis is still unknown, the current treatment is far from satisfactory. Thus, there is an urgent need to find a more effective therapy for this disease.

Decreased expression levels of complement regulator CD55 contribute to the development of bullous pemphigoid.

Bullous pemphigoid is a common autoimmune blistering disease of the elderly associated with autoantibody-mediated complement activation, and complement dysregulation is critical for its pathogenesis. As a crucial regulator of the complement system, CD55 has been widely studied in autoimmune diseases. Here, we investigated the involvement of CD55 in bullous pemphigoid, as little is known regarding its role in this disease.

Anti-collagen XVII single-chain Fv antibody blocks the autoimmune reaction mediated by pathogenic autoantibodies in bullous pemphigoid.

Background: Pathogenic autoantibodies in bullous pemphigoid (BP) recognize the non-collagenous 16A domain (NC16A) of collagen XVII (COL17), a hemidesmosomal component at the skin membrane. This immune inflammation involves activation of the complement cascade via the classical pathway. With similar antigen binding activity, Fab and single-chain variable fragments (scFv) of pathogenic anti-COL17 antibodies can interfere with COL17 binding of autoantibodies, blocking subsequent complement activation and granulocyte activation.