Different regulation of the L3T4-T cell subset by B cells in different mouse strains bearing the H-2k haplotype.

Splenic L3T4-T cells from Toxoplasma gondii-infected CBA/J (H-2k, Igh 1a) but not C3H/He (H-2k, Igh 1j) mice responded with marked antigen-specific proliferation and interleukin 2 (IL 2) production, as well as concanavalin A-induced proliferation. The proliferative response of C3H/He spleen cells could be restored in part in vitro by addition of exogenous recombinant IL 2. The observed unresponsiveness of C3H/He spleen cells was due to the release of IL 2-inhibiting factors. These factors, present in culture supernatants from antigen restimulated C3H/He spleen cells, blocked the growth of an IL 2-dependent T cell line in the presence of optimal concentration of IL 2. During the early stages of infection, C3H/He splenic macrophages lacked the capacity to present antigen. In addition a nonspecific B cell-mediated suppression of T cell proliferation was observed. In later stages of infection macrophages displayed normal antigen-presenting function in comparison with macrophages of normal uninfected mice. At this stage of infection nonspecific, minor histocompatibility restricted B cell suppression was observed. These results suggest a possible role of B cells in regulation of T cell immunity to T. gondii.