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The Myelin oligodendrocyte glycoprotein (MOG) peptide-MHC class II complex is a critical autoantigenic target involved in the pathogenesis of demyelinating diseases such as Multiple Sclerosis (MS). MOG is a glycoprotein located on the outermost surface of myelin sheaths in the central nervous system, making it highly accessible to the immune system. When MOG-derived peptides, particularly the immunodominant MOG35-55 epitope, are presented by MHC class II molecules on antigen-presenting cells, they trigger the activation and proliferation of autoreactive CD4+ T cells. These T cells orchestrate an inflammatory response that leads to myelin destruction and axonal damage. In therapeutic contexts, this complex is targeted by tolerogenic vaccines and antigen-specific therapies designed to reprogram the immune system. By delivering the MOG peptide in a non-inflammatory context, these treatments aim to induce immune tolerance, either by deleting the pathogenic T cells or by promoting the development of regulatory T cells that suppress the autoimmune attack.
Induction of antigen-specific immune tolerance through the deletion or anergy of autoreactive CD4+ T cells or the expansion of antigen-specific regulatory T cells (Tregs).
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