1404 T Cell Development in B Cell - Deficient Mice

The cellular interactions in the anti-p-azobenzenearsonate (ABA) 1 suppressor T cell pathway, for the inhibition of ABA-specific delayed-type hypersensitivity and cytotoxic T cell responses, are restricted by Igh-linked genes (reviewed in 1). The inducer, Ts-1 (T suppressor cell), and the effector, Ts-3, suppressor T cells, and one of their factors (TsF1) bear the major crossreactive idiotypic (CRI) determinants recognized by rabbit antiidiotypic antibodies prepared by immunizing rabbits with purified anti-ABA from appropriate strains of mice (2, 3). The presence of these Ig idiotypic specificities on T cells is not the result of the expression of Ig heavy chain variable region genes in T cells, but rather reflects the degree to which the repertoire of these regulatory T cells is influenced by the Ig idiotypes on B cells during their differentiation or induction. We therefore proposed (4) that clonal expansion of a B cell subpopulation bearing a particular idiotypic specificity stimulates the clonal expansion of corresponding antiidiotypic T or B cells. These antiidiotypic T or B cells, in turn, select and trigger the expansion of a population of idiotype-bearing T cells. Therefore, the detection of Ig idiotypes on T cells may merely reflect a serological or conformational crossreactivity, and represent internal images of B cell idiotypic specificities rather than a true genetic identity. This hypothesis is supported by findings indicating that certain T cell activities appear to depend on B cells for their expression (reviewed in 5). These include idiotype-specific helper T cells (6, 7), isotype-specific helper T cells (8), and antigen-specific proliferating T cells (9, 10). Moreover, it has recently been shown (11) that B cell-deficient mice are unable to produce one of the two chains comprising the T cell-derived, sheep red blood cell-specific inducersuppressor factor. Taking advantage of our previous observations (1) of the expression of antiCRI-def ined idiotype by Ts-1 ceils and their factors (TsF1) in the ABA-system, we studied whether the presence of Ig-bearing B cells is required for the