Abstract
B cells could be stimulated to proliferate by mitomycin C‐treated normal T cells that were activated by rabbit anti‐mouse brain antiserum (RaMBr). The B cell proliferation peaked 48 h after the initiation of the cultures. The T cell subset involved was Lyt‐1^+^, 2^−^. The B and T cells participating in the interaction did not need to be matched at the H‐2 locus. A long‐term T cell line (C.1.a), which was genetically restricted by the H‐2 complex in its antigen (ovalbumin)‐specific interaction with B cells, could also be induced by RaMBr to stimulate B cell proliferation. However, the RaMBr‐mediated interaction of C.1.a with B cells was genetically unrestricted. This suggests that T cell activation by RaMBr can bypass the requirement for the recognition of I region antigens, which is a feature of antigen‐specific interactions between T and B cells. In fact, RaMBr antibody appeared to function by bringing T cells into contact with B cells by the interaction of the B cell surface membrane Fc receptors with the Fc portion of RaMBr antibody bound to the T cell surface. Brain‐associated antigen(s) appeared to play a unique role in T‐B cell interactions because antibodies against other T cell surface antigens were inactive, e.g. those which remained in rabbit anti‐mouse thymocyte antiserum at a high titer after absorption with mouse brain tissue. Furthermore, the brain‐associated T cell antigen involved in the cellular interaction was differentiated from the Thy‐1 antigen by the failure of xeno‐anti‐Thy‐1.1 antisera to induce the interaction of B6.PL.Thy‐1^2^ T cells with B cells, and the presence of activity in rat anti‐AKR mouse brain serum which did not contain antibodies against Thy‐1.1 or Thy‐1.2 determinants.
The data appear to support the hypothesis that the brain‐associated T cell antigen, as defined serologically in these studies, may represent a molecule which plays a role in the immunological functions of the Lyt‐1^+^, Lyt‐2^−^ T cell subset.