Inherited polymorphism of the human T-cell antigen receptor detected by a monoclonal antibody.

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Abstract
Three different murine monoclonal antibodies to the human clonotypic T-cell antigen receptor immunoprecipitate the alpha-beta chain heterodimer; induce comodulation of the clonotypic molecule with the T3 molecular complex; stain small populations of normal polyclonal T cells, suggesting that they react with variable or joining region determinants of the clonotypic receptor; and induce proliferation of resting T cells. While two of these antibodies detect the clonotypic receptor in all individuals studied, the third antibody (OT145), described herein, does not detect the T-cell antigen receptor on T cells of all individuals. By indirect immunofluorescence, three groups can be distinguished within a population of individuals (n = 138) by OT145. Individuals lacking T cells reactive with OT145 have a homozygous OT145-phenotype. T cells from such individuals fail to proliferate in the presence of OT145 in contrast to T cells from OT145+ individuals. Individuals with a relatively large percentage of OT145+ T cells, 4.5 +/- 1.54% (mean +/- 2 SEM) are homozygous OT145+, while those with an intermediate percentage, 2.04 +/- 0.9%, have a heterozygous phenotype. Family studies suggest autosomal codominant inheritance of the OT145 phenotype. The distribution of the three OT145-defined phenotypes varies considerably in populations of different ethnic background. Taken together these data suggest that the polymorphism detected by OT145 may represent a variable or joining region allotypic system of the human T-cell antigen receptor. In addition, our results indicate that allelic exclusion governs the expression of the clonotypic receptor by human T cells.