Some immunobiological aspects of host responses to an immunosuppressive protein (p36) released by porcine monocytes upon infection with African swine fever virus were analysed in a murine system. Treatment of normal, adult C57BL/6 mice with p36 (i) significantly delayed allogenic skin graft rejection; (ii) suppressed the specific plaque-forming cell response to immunization with heterologous erythrocytes; but (iii) induced marked increases in the numbers of 'background' splenic Ig-secreting plaque-forming cells. Cytofluorometric analysis of spleen cells revealed that a considerable fraction of all B cells, as well as CD4 and CD8 T lymphocytes, undergo blast transformation after p36 treatment. The immunosuppressive effects do not seem to result from 'antigenic competition', for they cannot be induced by even higher doses of pig albumin or by culture products of non-infected pig monocytes. Suppression of specific antibody responses and stimulation of 'background' plaque-forming cells are both T cell-dependent, since they are markedly reduced in thymectomized mice and in animals treated with anti-CD4 or anti-CD8 antibodies. This suggests the relationship between non-specific stimulation and specific suppression of 'unrelated' immune responses and reinforces the notion that viral-associated immunosuppression may be due to overstimulation. The present murine experimental model may prove valuable in the study of immunosuppression associated with infection, even for microorganisms which do not infect mice.
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