DA (RT1a) hearts were transplanted into PVG (RT1c) or DA recipients, excised on days 1, 3, 5, or 7 after grafting, and examined by immunohistological techniques and quantitative absorption analyses, using allospecific mouse anti-rat class I and class II major histocompatibility complex (MHC) monoclonal antibodies. Cryostat sections stained by the peroxidase technique demonstrated that, in the normal heart, class I antigens were largely restricted to vascular endothelium and interstitial cells, with no observable staining of the myocardial cells except at the intercalated discs. Class II antigens were found only on occasional interstitial dendritic cells. The picture at day 1 after transplantation was not noticeably different. By day 3, however, there was clear patchy induction of both class I and class II antigens on the myocardial cells, usually in the region of cellular infiltrates. By day 5, class I antigens had been strongly induced throughout the graft, with the myocardial cells being very strongly positive. Class II antigens were also uniformly expressed on myocardial cells at day 5, and at this stage the vascular endothelium was also strongly positive. Quantitative absorption analyses showed a 10-fold increase in class I antigen content in cardiac allografts at day 5 after transplantation when compared with normal DA heart. DA heart isografts showed no increase in class II antigens, but it was interesting that, by 5 d after grafting, there appeared to be some expression of class I antigens on the myocardial cells. Quantitative absorptions showed a threefold increase in class I antigens on 5-d isografts when compared with normal DA heart.
Massive induction of donor-type class I and class II major histocompatibility complex antigens in rejecting cardiac allografts in the rat.
A D Milton, J W Fabre; Massive induction of donor-type class I and class II major histocompatibility complex antigens in rejecting cardiac allografts in the rat.. J Exp Med 1 January 1985; 161 (1): 98–112. doi: https://doi.org/10.1084/jem.161.1.98
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