Antigen-specific helper T cells required for dominant idiotype expression are not H-2 restricted

Abstract

Two synergizing antigen-specific helper T (Th) cell populations are required for an optimal TEPC15 (T15)-dominated antiphosphorylcholine (PC) plaque-forming cell response. In these studies, the 2 Th cell sets are shown to differ in their requirements for recognition of self-major histocompatibility complex (MHC)-encoded determinants by testing the ability of Th cells from F1 .fwdarw. parent bone marrow chimeras to collaborate with PC-specific B cells bearing MHC-encoded determinants of either parental haplotypes. Previous studies showed that 1 antigen-specific Th cell population is required for T-dependent anti-PC responses and activates PC-specific B cells only if the hapten, PC, is physically linked to the priming antigen. This Th cell, referred to as ThMHC, induces anti-PC responses that are mainly non-T15 in character and it appears to be identical to the conventional antigen-specific Th cell. In these experiments, using T cells from (A .times. B)F1 .fwdarw. parent A chimeras, ThMHC cells requiring hapten-carrier association provide help for F1 and parent A B cells but not for B cells from parent B, thus confirming that the activity of the conventional Th cell is H-2 restricted. The 2nd antigen-specific Th cell population, whose function is measured in the presence of the ThMHC cell set, preferentially activates T15-bearing B cells. This Th cell set (ThId) is missing in mice expressing low levels of T15-bearing antibody and can be restored by the addition of antigen-specific T cells from donors expressing high levels of circulating T15 Id. T cells from T1 .fwdarw. parent chimeras that express substantial levels of T15-bearing anti-PC antibody could evidently provide ThId cell activity for the selective activation of T15-bearing B cells of F1 and both parental H-2 types. Although the activity of conventional (ThMHC) cells is clearly H-2 restricted, ThId cells from the same chimeric donors are not required to recognize antigen in association with self-MHC-encoded determinants for successful T-B collaboration.