T cell receptor recognizing modified Myelin Oligodendrocyte Glycoprotein (TCR-modified MOG)

T cell receptors (TCRs) recognizing modified Myelin Oligodendrocyte Glycoprotein (MOG) or related self-peptides are critical mediators of neuroinflammatory autoimmune diseases such as Multiple Sclerosis (MS) and MOG-antibody disease (MOGAD). MOG is a minor component of the central nervous system myelin sheath, but it is highly encephalitogenic, serving as a primary target for autoreactive CD4+ and CD8+ T cells. Modifications to MOG peptides, such as citrullination or oxidation, can enhance their immunogenicity or allow them to bypass central tolerance, leading to the activation of pathogenic T cell clones. Furthermore, these TCRs often exhibit cross-reactivity with environmental antigens (molecular mimicry), which can trigger or exacerbate the autoimmune response. Therapeutic strategies targeting these receptors aim to restore immune tolerance through the use of altered peptide ligands (APLs), tolerogenic vaccines like OM-MOG35-55, or the depletion of specific autoreactive populations using CAR-T cell technologies. Monitoring the frequency and cytokine profile (e.g., IFN-gamma, IL-17) of MOG-specific T cells serves as a vital biomarker for disease activity and therapeutic efficacy.

Other names

MOG-reactive T cell receptorMyelin-reactive T cell receptorCross-reactive MOG TCRModified MOG-specific TCREncephalitogenic T cell receptor

Induction of antigen-specific immune tolerance, deletion of pathogenic autoreactive T cells, or expansion of regulatory T cells (Tregs) to suppress neuroinflammation.