CORRELATION OF IMMUNOLOGICAL FUNCTION WITH SPLENIC HISTOPATHOLOGY DURING THE PRECLINICAL STAGES OF HOST-VERSUS-GRAFT SYNDROME IN PAR-ENT-F1 MOUSE CHIMERAS

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Abstract
Host-versus-graft syndrome is a fatal disease complex induced in parent strain mice by perinatal inoculations of F1 hybrid spleen cells and manifested by thrombocytopenia, intestinal hemorrhage, massive lymphosplenomegaly, thymic atrophy, and renal disease that resembles human membranous glomerulonephropathy. The pathogenesis of the disease was investigated by simultaneous studies of the immunological and morphological responses of young experimental mice in the preclinical stages of the disease. The early hemolytic plaque-forming responses of RFM/(T6 RFM)F1 mice to sheep red blood cells were significantly elevated above those of controls, and correlated with precocious development of germinal centers with their coterie of B lymphocytes. The premature appearance of these structures was most likely induced by the semiallogeneic F1 hybrid cells. Later, the impaired plaque-forming responses observed in experimental mice correlated best with lack of T lymphocytes. Depletion of these cells accompanied an acute inflammatory cellular infiltrate which was quite severe in thymic-dependent areas of splenic white pulp, but which was absent from the germinal centers. Work on both host-versus-graft and graft-versus-host syndromes has made it increasingly clear that premature exposure of the immune response system to allogeneic and semiallogeneic cells is a potentially lethal event.

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