Mice injected from day of birth onwards with rabbit anti‐mouse IgM (anti‐μ) antibodies were found to be B cell‐deficient and defective for the induction of antigen‐reactive proliferating T cells (TPRLF). This defective induction was not due to the absence of circulating antigen‐specific antibodies since the daily injections of such antibodies during exposure to antigen did not restore the ability of anti‐IgM treated animals to generate TPRLF. Analyzing the cellular events implicated in the induction of virgin antigen‐reactive T cells, anti‐μ‐treated mice manifested impairment of the three interacting cell types involved in the induction of TPRLF. Thus, peritoneal and splenic antigen‐presenting cells from such animals were impaired in their capacity to signal a primary antigen‐specific T cell reaction. Their splenic lymphocytes could not function as initiator cells in transferring immunogenic signals to recruit TPRLF in normal recipients. Potent antigen‐specific splenic initiator cells failed to induce the recruitment of specific TPRLF in anti‐μ‐treated mice. The defective induction of TPRLF in anti‐μ‐treated mice may be due to a functional impairment of cells expressing membranebound IgM molecules which seemingly play a central role in the transfer of immunogenic signals for the recruitment of antigen‐specific circulating T cells. We suggest that splenic B cells function as initiators in the transfer of antigen‐induced signals from peritoneal antigen‐presenting cells to T cells. These seems to be the primary targets of anti‐μ treatment.
ASJC Scopus subject areas
- Immunology and Allergy