On the implications of polyclonal B cell activation.

The mechanism of polyclonal activation suggested that it was the indirect and nonspecific result of cytokine release by either B cells stimulated by antigen or T cells stimulated by viral peptide bound to major histocompatibility complexes (MHCs) on antigen-presenting cells (APCs). The mechanism proposed by researchers however, differs by postulating that virusspecific CD4 cells interact with viral peptide-MHC complexes exposed on the surface of B cells acting as APCs and directly stimulate these B cells to differentiate, regardless of their BCR specificity. Authors suggest that the phenomenon of polyclonal B cell activation is much more general and wish also to comment on some further theoretical implications of their study. T cells may also be engaged in non-specific polyclonal activation. Thus, only a small proportion of passively administered specific T cells is found in the infiltrates that mediate skin graft rejection or delayed-type hypersensitivity. The implication of these findings is that any specific antigenimmunocyte interaction may serve the purpose. Researchers have suggested that this phenomenon is an important contributor to the luxuriant mononuclear infiltrates found in all immunogenic inflammatory reactions involving B and T cells.