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Diversity of T-cell receptor V_alpha, V_beta, and CDR3 expression by myelin basic protein-specific human T-cell clones

From the Departments of Neurology (Dr. Richert and E. Robinson, K. Camphausen, and M. Faerber) and Microbiology and Immunology (Drs. Richert and Hurley), Georgetown University Medical Center, Washington, DC; and the Neuroimmunology Branch (Drs. Martin, Voskuhl, and McFarland), NINDS, National Institutes of Health, Bethesda, MD.
Supported by NIH grant RO1AI26675, National Multiple Sclerosis Society grant RG1769-C-5, the Straus Fund, and Division of Research Resources BRSG RR5360.
Received September 26, 1994. Accepted in final form March 8, 1995.
Address correspondence and reprint requests to Dr. John R. Richert, Department of Neurology, Georgetown University Medical Center, 3800 Reservoir Road, NW, Washington, DC 20007.

We sequenced the cDNAs of alpha and beta T-cell receptors (TCRs), including V, J, and CDR3 regions, expressed by 54 myelin basic protein (MBP)-specific T-cell clones generated from the peripheral blood of 15 multiple sclerosis (MS) patients and three normal controls. Thirteen V_alpha gene segments, 18 V_beta gene segments, 23 CDR3_alpha sequences, and 30 CDR3_beta sequences were represented among these clones. Some CDR3 motifs were common to several clones that shared epitope specificity, while other motifs were common to clones with diverse epitope specificities. The extensive heterogeneity of TCR gene expression in the human immune response to MBP indicates that therapeutic strategies aimed at blocking a limited number of TCRs are unlikely to fully suppress the T-cell response to MBP in vivo.

NEUROLOGY 1995;45: 1919-1922

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