From specificity to degeneracy to molecular mimicry: antigen recognition of human autoreactive and pathogen-specific CD4+ T cells
Multiple sclerosis (MS) is a chronic demyelinating disease of the central nervous system (CNS). Although the cause of MS has not been identified, it is widely believed that myelin-specific T cells are somehow involved in the disease process . However it is not clear how these cells become activated and mediate CNS disease. One of the most attractive models for the activation of autoreactive T cells is termed the “molecular mimicry hypothesis” . According to this model, autoreactive T cells become activated in the peripheral immune system by crossreactive ligands derived from infectious agents. After activation and upregulation of adhesion molecules, these cells can cross the blood-brain barrier; after reactivation by myelin antigens either directly or via the recruitment of other cells, the activated T cells damage the myelin sheath and oligodendrocytes.
KeywordsMyelin Basic Protein Molecular Mimicry Peptide Library Antigen Recognition Optimal Amino Acid
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