The objectives of this proposal are to define the biological mechanisms responsible for determining the idiotopic specificities and Igh restrictions of suppressor T cells and the possible mechanism by which B cells and their products may influence these specificities. To accomplish these goals, three specific approaches will be evaluated. The first will involve administration of anti-mu antisera and anti-idiotypic antisera from birth to selected strains of inbred mice to determine the consequence of suppression of B cell differentiation and growth on the Igh restriction specificity of suppressor T cells in the azobenzenearsonate system.
The second aim of this study will be to evaluate the influence of B cells in early events in T cell differentiation through the construction of bone marrow chimeras using reconstitution with selected allotype mismatched bone marrow populations. We will subsequently evaluate the nature of T cell restriction in terms of Igh-1 genetic restriction of suppressor cells derived from these chimeric mice and related these results to those which have been previously described in the azobenzenearsonate system. The third part of the proposal will be to evaluate the Igh restriction and idiotype specificities on T suppressor cells from Igh-1a BALB/c mice, which have been immunologically manipulated to express subsets of B cells expressing the appropriate cross-reactive idiotype. Suppressor T cells will be induced in such mice and idiotypic phenotype and restriction specificities evaluated. It is the intent of this project to examine those relationships which exist between B and T cells during early events of differentiation which may have a significant impact on subsequent Igh-linked restricted interactions and expression of specific idiotypic specificities.
