In the accompanying paper we shoed that the injection of BALBc mice with 800 mu g of GaM delta induced a direct polyclonal increase in B cell proliferation as well as an indirect increase in T cell proliferation. This led us to investigate whether the same treatment might lead to polyclonal Ig secretion. We found that 6 to 7 days after GaM delta injection one-quarter to one-half of splenic B lymphocytes lost detectable surface IgM and acquired surface IgG. Surface labeling experiments established that much of this IgG had the electrophoretic characteristics of membrane rather than serum IgG, and was, therefore intrinsic rather than cytophilic. GaM delta also induced a striking increase in Ig secretion 6 to 7 days after injection, as indicated by 1 an approximately eightfold increase in serum IgG1 levels and smaller increases in serum IgM and IgG2a levels 2 greater than fivefold and 50-fold increases in the in vitro incorporation of 3H-leucine into IgM and IgG, respectively, by spleen cells from GaM delta-injected mice and 3 three to 10-fold and 20 to 50-fold increases in the percentages of spleen cells with large amounts of intracytoplasmic IgM and IgG, respectively. The great majority of the increase in cell surface and secreted IgG was accounted for by an increase in the IgG1 subclass. Both absorption and plaquing studies indicated that the increase in Ig secretion and plaquing studies indicated that the increase in Ig secretion was polyclonal rather than a specific immune response to goat Ig. The injection of anti-delta antibodies failed to induce B cells from congenitally athymic mice or mice that were tolerant to the injected anti-delta antibody to undergo a switch in cell surface isotype or to differentiate into antibody-secreting cells. We interpret these data and data presented in the companion paper as suggesting the binding to and crosslinking of B cell surface IgD by ligand leads to 1 direct activation of B lymphocytes that can include...

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