Inhibition of Azobenzenearsonate Sensitivity

When A/J mice are immunized to p-azobenzenearsonate (ABA) 1 coupled to a protein, such as keyhole limpet hemocyanin (KLH), 20-70% of the anti-ABA antibodies produced bear a common idiotype, known as the cross-reactive idiotype (CRI; 1, 2). CRI is absent in the serum of A/J mice immune to antigens other than ABA. In many other mouse strains, immunization with ABA-KLH results in high levels of anti-ABA antibodies hut these lack the CRI, the expression of which is linked to the CH gene cluster (3, 4). The CRI is thus a genetic marker for the V regions of immunoglobulin (Ig) of the A/J strain. The presence of CRI has also been demonstrated on T cells, such as suppressor T cells induced by the injection of ABA-coupled syngeneic spleen cells (5) and on suppressor factors derived from these (6). Mice from strains that lacked the gene coding for the CRI also produced factors specific for ABA but devoid of CRI. The involvement of the specific VH gene for the CRI in coding not only for antibodies with ABA specificity but also for ABA-specific suppressor T cell factors was thus inferred. To study the existence of CRI on immune T cells, we produced contact sensitivity to ABA and examined the interaction of sensitized cells with ABA-conjugated spleen cells in vitro. Sensitization produced at least two separate T cell activities restricted by different regions of the major histocompatibility complex (MHC). One of these was H-2I restricted and responsible for the successful transfer of sensitivity to naive recipients. The other was revealed after in vitro interaction of sensitized cells with antigen-conjugated cells. It was H-2K restricted and inhibitable by soluble antigen or by anti-CRI antibody. Sensitization with ABA thus induced C R I ÷ T cells able to participate in idiotype-anti-idiotype-driven regulatory mechanisms, regardless of whether T cells mediating contact sensitivity were themselves CRI +.