Helper Cells Are Restr icted to Coopera te wi th B Cells Expressing the IgVH Pheno type of the Pr iming B Cells

The humoral immune response to heterologous erythrocytes requires the cooperation of B lymphocytes and helper T cells. The production of anti-sheep erythrocytes (SRBC) 1 IgG is almost wholly dependent on the activity of T help (reviewed in 1). Helper T cells that recognize the carrier portion of an immunogen have been known for some time (2). More recently evidence has accumulated that other helper T cells exist that recognize autologous Ig structures (3) such as allotype (4), isotype (5, 6), or idiotype (7-10). Previously it was shown that intravenous transfer of polyclonally stimulated B cell blasts induces activation of syngeneic Lyt-1÷,2-,3 T cells (11). Removal of surface Ig (sIg) by capping abolished the capacity of B cell blasts to activate Lyt-1 + T cells. It seemed possible that this activation of Lyt-1 + T cells by Ig-associated structures on B cells might represent the triggering of Ig-specific helper T cells. The aim of this report is to present findings of experiments testing the hypothesis that antigen-activated B cells display or produce Ig-associated structures that trigger T cells that have receptors specific for these molecules. These triggered T cells would give rise to clones of helper cells specific for B cells displaying Ig-associated molecules similar to those on the priming B cells. To study this, I used B cells from mice recently immunized with SRBC and tried to determine if these B cells could induce T helper cells capable of helping the humoral response to SRBC. I tried to determine whether (a) there is any genetic restriction such that the activating B cells and the helper T cells had to share Ig heavy chain (Igh) alleles or if (b) the specificity of the T helper cells is generated by recognition of structures associated with the priming B cells that are either encoded by genes linked to the loci for the variable (IgvH) or constant (IgcH) part of the immunoglobulin heavy chain.