Requirement for B cell-derived immunoglobulin for T_H activation by the type 2 antigen polyvinylpyrrolidone

T_h specific for the type 2 antigen potyvlnylpyrrolldone (PVP) could not be activated in vivo or in vitro In mice rendered B cell deficient by treatment from birth with antl-lgM. The requirement for B cells was apparently not due to a requirement for B cells to function as antigen presenting cells for T_h activation since T cells also were not activated when antl-lgM treated mice were reconstituted with B cells prior to priming with PVP. In addition, removal of B cells from spleens of adult of adult mice had no effect on the ability of PVP to activate T_h in vitro. Potential nonspecific effects of chronic antl-lgM treatment on T cell function are unlikely since T cells from antl-lgM treated mice provided help to B cells for antibody responses to horse red blood cells responded normally to T cell mltogens and had a CD4:CD8 ratio like that of untreated mice; PVP primed T cells from anti-IgM treated mice also did not actively suppress the helper activity of PVP primed T cells from normal mice. In addition, PVP-speclflc T_h were able to be activated in mice given multiple injections of antl-lgM beginning 2 weeks after birth and in mice given MOPC 104E IgM together with antl-lgM; under these conditions B cell depletion by the anti-IgM did not occur. Thus activation of PVP-speclflc T_h requires that B cells be present during the first few weeks after birth. Experiments in which mice were given injections of normal mice Ig together with the antl-lgM indicate that the function of B cells for T_h activation in this system can be replaced by B cell-derived Ig. Thus PVP-speclfic T_h could be activated in mice treated from birth with antl-lgM plus normal Ig despite the absence of significant numbers of B cells in the spleens of these mice.