CNTN2 (Contactin-2), also known as TAG1 (Transient Axonal Glycoprotein-1), is a cell adhesion molecule belonging to the immunoglobulin superfamily. It plays a critical role in nervous system development, including axon guidance, myelination, and synapse formation. CNTN2/TAG1 is predominantly expressed in the paranodal regions of myelinated axons and interacts with proteins like contactin-associated protein 1 (Caspr1) to maintain structural integrity and facilitate signal transduction.
Antibodies targeting CNTN2/TAG1 are primarily studied in the context of autoimmune neurological disorders. They have been implicated in autoimmune neuropathies, such as chronic inflammatory demyelinating polyneuropathy (CIDP) and Guillain-Barré syndrome (GBS), where aberrant immune responses attack peripheral nerve components. These autoantibodies may disrupt paranodal junctions, impairing saltatory conduction and leading to neuromuscular dysfunction. Recent studies also associate CNTN2/TAG1 antibodies with paraneoplastic neurological syndromes, particularly in malignancies like thymoma or lymphoma, suggesting a potential molecular mimicry mechanism.
Detection methods include cell-based assays (CBA) and tissue immunohistochemistry. Clinically, their presence may correlate with specific phenotypes, such as sensory ataxia or severe motor weakness, influencing treatment choices (e.g., immunotherapy responsiveness). Research continues to explore their pathogenic role and diagnostic utility in autoimmune neurology.