Myelin basic protein 83-99-specific T-cell receptor (MBP83-99-specific TCR) (MBP83-99-specific TCR)

The Myelin basic protein 83-99-specific T-cell receptor is a specialized immune receptor found on the surface of T lymphocytes that recognizes a specific immunodominant fragment of myelin basic protein (MBP) presented by MHC class II molecules, particularly HLA-DR2 (HLA-DRB1*15:01) (Krogsgaard et al., 2000, Nature). In the context of Multiple Sclerosis (MS), these TCRs play a critical role in the pathogenesis of the disease by mediating the autoimmune attack on the myelin sheath within the central nervous system (Ota et al., 1990, Nature). Therapeutic strategies targeting these receptors aim to selectively silence or eliminate the pathogenic T-cell clones without compromising the broader immune system. This is achieved through various approaches, such as altered peptide ligands (APLs) like NBI-5788 that act as TCR antagonists or partial agonists to shift the immune response from a pro-inflammatory to a regulatory state (Bielekova et al., 2000, Nature Medicine). Other interventions include TCR-peptide vaccines like NeuroVax, which induce anti-idiotypic regulatory responses against specific TCR V-beta chains commonly used by MBP-reactive cells (Vandenbark et al., 2008, Journal of Neuroimmunology). Monitoring the frequency and activation state of T cells expressing these specific TCRs serves as a vital biomarker for disease activity and therapeutic efficacy in MS clinical trials (Hellings et al., 2001, Journal of Neuroscience Research). Additionally, soluble MHC-peptide complexes are being explored to directly target and induce anergy in these specific T-cell populations.

Other names

MBP(83-99)-specific TCRMyelin basic protein peptide 83-99-specific T-cell receptorAnti-MBP83-99 TCRMBP83-99-reactive T-cell receptor

Antigen-specific immune modulation including TCR antagonism, induction of T-cell anergy, and stimulation of anti-idiotypic regulatory T-cell responses to suppress myelin-reactive T-cell populations (Bielekova et al., 2000, Nature Medicine; Vandenbark et al., 2008, Journal of Neuroimmunology).