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Molecular Mimicry in Neurological Diseases

National Institute for Neurological Diseases and Stroke, Bethesda, Maryland, silva{at}box-s.nih.gov

Several mechanisms have been implicated in the activation and expansion of myelin-specific T cells in multiple sclerosis, a presumed autoimmune disease of the central nervous system. In this article, we will review the mechanisms of molecular mimicry whereby myelin-specific T lymphocytes may be activated by foreign antigens. Recent studies from our laboratory have documented an unexpected flexibility of T cell receptor recognition and demonstrated that sequence homology is not a requirement for cross-recognition. Using synthetic combinatorial peptide libraries, it was possible to identify the entire spectrum of molecular mimics for T cell clones. This approach may prove useful for the development of antigen-specific therapies and vaccines.

Key Words: Molecular mimicry • Cross-reactivity • T cell receptor specificity

The Neuroscientist, Vol. 6, No. 6, 428-432 (2000)
DOI: 10.1177/107385840000600605


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