Myelin-based autoantigen-specific T-cell pathways

Myelin-based autoantigen-specific T-cell pathways are the central drivers of neuroinflammation in Multiple Sclerosis (MS). These pathways involve the activation of CD4+ and CD8+ T-cells that recognize specific epitopes of myelin proteins, including Myelin Basic Protein (MBP), Proteolipid Protein (PLP), and Myelin Oligodendrocyte Glycoprotein (MOG) (Source: PubMed, PMID: 31558731). Once activated, these cells infiltrate the central nervous system, releasing pro-inflammatory cytokines and recruiting other immune cells that destroy the myelin sheath (Source: NIH, StatPearls - Multiple Sclerosis). Therapeutic strategies targeting these pathways, known as antigen-specific immunotherapies (ASIT), seek to induce peripheral tolerance or immune deviation. By administering myelin-derived peptides or altered peptide ligands, these therapies aim to expand regulatory T-cell (Treg) populations or induce anergy in pathogenic T-cells, potentially offering a more precise and safer alternative to systemic immunosuppression (Source: Nature Reviews Neurology, doi:10.1038/s41582-019-0222-2). Drugs like Glatiramer acetate act as decoy antigens to shift the immune response from a pro-inflammatory state to an anti-inflammatory state, thereby protecting the neural tissue from further autoimmune damage (Source: PubChem, CID: 3081884).

Other names

Myelin-reactive T-cell pathwaysAutoreactive myelin-specific T-cell responseMyelin-specific T-cell activationAntigen-specific T-cell pathways in Multiple Sclerosis

Induction of immune tolerance, T-cell anergy, and regulatory T-cell (Treg) expansion through antigen-specific presentation and MHC competition.