REQUIREMENT FOR B-CELL-DERIVED IMMUNOGLOBULIN FOR T(H) ACTIVATION BY THE TYPE-2 ANTIGEN POLYVINYLPYRROLIDONE

T(h) specific for the type 2 antigen polyvinylpyrrolidone (PVP) could not be activated in vivo or in vitro in mice rendered B cell deficient by treatment from birth with anti-IgM. 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 anti-IgM 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 non-specific effects of chronic anti-IgM treatment on T cell function are unlikely since T cells from anti-IgM treated mice provided help to B cells for antibody responses to horse red blood cells responded normally to T cell mitogens 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-specific T(h) were able to be activated in mice given multiple injections of anti-IgM beginning 2 weeks after birth and in mice given MOPC 104E IgM together with anti-IgM; under these conditions B cell depletion by the anti-IgM did not occur. Thus activation of PVP-specific 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 anti-IgM indicate that the function of B cells for T(h) activation in this system can be replaced by B cell-derived Ig. Thus PVP-specific T(h) could be activated in mice treated from birth with anti-IgM plus normal Ig despite the absence of significant numbers of B cells in the spleens of these mice.