**Background of PLEC Antibodies**
Plectin (PLEC), a high-molecular-weight cytoskeletal protein, plays a critical role in maintaining cellular integrity by linking intermediate filaments, microtubules, and actin microfilaments. It also stabilizes cell-matrix adhesions and regulates signaling pathways. Autoantibodies targeting plectin, termed PLEC antibodies, are primarily associated with autoimmune blistering diseases, particularly **mucous membrane pemphigoid (MMP)** and **paraneoplastic pemphigus (PNP)**.
PLEC antibodies were first identified in patients with PNP, a rare, severe autoimmune disorder often linked to underlying malignancies. These autoantibodies disrupt plectin-mediated cytoskeletal organization, leading to epithelial detachment and blister formation. Detection methods include indirect immunofluorescence (IIF) on epithelial substrates and immunoblotting using recombinant plectin proteins.
Clinically, PLEC antibodies serve as diagnostic markers for specific autoimmune subtypes. Their presence may correlate with disease severity and poor prognosis, especially in PNP. However, PLEC autoimmunity remains less characterized compared to other target antigens (e.g., desmogleins). Research continues to explore their pathogenic mechanisms, epitope mapping, and potential therapeutic implications, such as targeting B-cell pathways. Despite progress, standardized assays and clinical validation are needed to optimize diagnostic and prognostic utility.