Adoptive transfer of a superantigen-induced hole in the repertoire of natural IgM-secreting cells

Abstract

We have recently evaluated the host response to the bacterial toxin, protein A from Staphylococcus aureus (SpA), which has the capacity to interact with B-cell antigen receptors encoded by V(H) clan III genes via a conserved variable region framework surface. In these studies, intraperitoneal instillation of SpA induced a persistent T-cell independent loss of a large supraclonal set of susceptible lymphocytes, which includes clan III/V(H) S107 family-expressing B-1 cells and their antibody products. To determine whether these long-term effects could represent the influence of residual in vivo deposited superantigen, we have now performed adoptive transfer of peritoneal B cells from superantigen- and control-treated donors. These studies demonstrated that mice that received cells from SpA-treated donors also exhibited the same induced supraclonal hole in the expressed repertoire of natural IgM-secreting cells due to supraclonal deletion. These studies clarify the cellular mechanisms responsible for B-cell superantigen-induced modification of the repertoires of in vivo polyclonal B-cell populations.