Antigenic competition between heterologous erythrocytes in mice. Immunological and histological studies exploring mechanisms of the antigenic competition.

To explore the mechanisms of antigenic competition, immunological and histological studies were made on mice using non-crossreacting heterologous erythrocyte antigens, i.e. sheep (SRBC), horse (HRBC) and chicken (CRBC) erythrocytes. Deficiency in the competition-inducing capacity of CRBC which we demonstrated in a previous paper was corroborated by the results that under any experimental conditions examined CRBC were unable to induce the competition. Of interest in the studies was that when anti-HRBC antibody responses of mice pre-injected with SRBC, i.e. competing antigen, were examined on day 2 and day 4 of HRBC-immunization, the day-2 response was revealed to be significantly enhanced, whereas the day-4-response was markedly suppressed as a result of the antigenic competition. By contrast, pre-injection with CRBC, i.e. non-competing antigen, did not affect at all either day-2 or day-4 anti-HRBC response of mice. Histological features of the spleens of mice either being prepared for antigenic competition or undergoing competitively suppressed antibody response were characterized by prominent regeneration of hyperplastic germinal centres, involving appearance of numerous tingible bodies and distinct collars of small lymphocytes which suggested massive proliferation and degeneration of lymphocytes. The spleens of mice in the immunological state indifferent to antigenic competition were characterized by huge lymphatic follicles which contained very few tingible bodies and were circumscribed by a markedly attenuated zone of small lymphocytes. From all these results, we suggest that massive proliferation and differentiation of T lymphocytes, probably toward regulatory (suppressor) T cells, could account for a mechanism of antigenic competition, and that deficient competition-inducing capacity of CRBC should be ascribed to weakness of their capacity in activation of the regulatory T lymphocytes.