Abstract
Intracardiac injection of lymph node cells into newborn allogeneic recipients incompatible with congenic donors at multiple loci within theH-2 complex (B10→B10.A) led to GVH splenomegaly, retarded growth, and mortality. In contrast,H-2I region differences [B10.A(4R)→B10.A(2R)] required fortyfold more cells to produce a comparable splenomegaly, and did not produce runting or GVH mortality despite a strong proliferative response in the spleen. However, when 4R donors were preimmunized with host lymphoid cells, 51 percent of 2R recipients died of allogeneic disease. GVHR was also observed in the reciprocal combination (2R→4R), in contrast to previous reports. The phenotypic determinants governing GVHR in the 4R→2R combination are probably coded for byI-C subregion genes. Disparities at theI-B orI-J subregions did not evoke detectable GVHR. The data indicate thatI-C subregion loci have the impact of so-called minor or moderate histocompatibility (MoH) loci. Possible implications for allogeneic human bone marrow transplantation are discussed.
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