PubMed1980
Mice injected with rat erythrocytes developed anti-erythrocyte autoantibodies which reached a plateau at 4-12 weeks, then gradually declined until at about 24 weeks the majority of mice were negative. In such recovered mice re-challenge with rat erythrocytes produced an accelerated peak of autoantibody and a much more rapid return to a Coombs' negative state. The auto-antibody response was distinguished from the anti-rat response in being more radio-sensitive. Purified autoantibody reacted to higher titre with rat than with syngeneic erythrocytes. Lymphoid cells, from mice given rat erythrocytes (but not sheep, rabbit or guinea-pig erythrocytes) transferred to normal syngeneic recipients given rat erythrocytes suppressed autoantibody production in the recipients. This suppression was much more effective against the autoantibody response than against the response to the inducing cross-reactive antigen; and the degree of suppression was related to the number of cells transferred and to their time of administration relative to the injection of rat erythrocytes. The induction of autoantibody and the generation of suppressor cells in donor animals was unaffected by adult thymectomy. A comparison of the effect of anti-rat erythrocyte antibodies and spleen cells from rat-immunized donors on recipients responses to rat erythrocytes revealed that whereas anti-rat antibodies suppressed both the autoantibody and the anti-rat responses, the spleen cells suppressed only the autoantibody response. Populations of spleen cells, from rat immunized donors, depleted of B cells retained their suppressive activity, whereas the suppressive efficacy of T-cell depleted populations was reduced but not abolished. It is suggested that T cells can specifically interfere with thesponse of autoreactive B cells, although non-T cells (possibly B cells acting by an antibody-feedback mechanism) can also suppress their response.