Definintion of antigen specific receptors on human T lymphocytes has been hampered by the extraordinary heterogeneity of these cells and the MHC restrictions which govern their activation. However, the recent development of clonal populations of antigen specific IL-2 dependent T cells and the availability of multiple monoclonal antibodies to T lineage specific surface glycoproteins make it possible to overcome these difficulties. To this end, we will examine the capacity of various monoclonal antibodies to indluence antigen spcific recognition and effector function of homogeneous T cell populations in the absence of complement. These will include monoclonal antibodies to nonpolymorphic determinants found on all mature T lymphocytes (anti-T1, T3, T3A, T3B, T11, T12), monoclonal antibodies to nonpolymorphic determinants selectively expressed on subsets of T cells (anti-T4, T4A, T4B, T4C, T8, T8A, T8B, T8C, etc.) and monoclonal antibodies to clonotypic (anti-idiotypic) determinants unique to individual clones. Utilizing cytotoxic T4 and T8 clones with defined MHC class II and class I target specificities, respectively, and noncytotoxic soluble antigen (KLH) specific clones we will define: 1) T cell surface molecules required for the recognition phase of CTL effector function in comparison with those employed in antigen specific recognition by noncytolytic clones; 2) the relationship of T cell function to the novel 20KD glycoprotein defined by anti-T3 antibodies which rapidly induce its modulation via external shedding; 3) the potential antigen binding properties of 35S-labelled T3 molecules and any comodulating structures; 4) the effect of clonotypic antibodies on enhancing or inhibiting function and growth of clonotype positive and negative clones, frequency and specificity of such clones, the relationship of structures defined by clonotypic antibodies and nonpolymorphic structures detected with anti-T3, anti-T4 and anti-T8, and the nature of the cellular clonal anti-clonal response; and 5) activation antigens expressed by one or another T celll subset, the relationship of activation structures to clonal function, and possible genetic polymorphism of these molecules.
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