Molecular mimicry and antigen-specific T cell responses in multiple sclerosis and chronic CNS Lyme disease.

摘要: The concept of molecular mimicry provides and elegant framework as to how cross-reactivity between antigens from a foreign agent with self proteins may trigger autoimmune diseases. While it was previously thought that sequence structural homology or the sharing T cell receptor (TCR) MHC-binding motifs are required for occur, we have shown even completely unrelated peptide sequences lead cross-recognition by cells. use synthetic combinatorial libraries in positional scanning format (PS-SCL) together novel biometric prediction approaches has allowed us describe recognition profiles individual autoreactive clones (TCC) unprecedented accuracy. Through studies myelin-specific TCC well nervous system patients suffering chronic central (CNS) Lyme disease become clear at least some cells more degenerate than anticipated. These data will not only help redefine what constitutes specific recognition, but also allow study detail biological role mimicry. A recent clinical trial an altered ligand (APL) one candidate myelin basic protein (MBP) epitopes MS (amino acids 83-99) such modified MBP therapeutic efficacy, bears potential exacerbate disease. Thus, provide firm evidence principles their pathogenetic significance relevant MS.