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( The Wistar Institute, Philadelphia 4, Pa.)
Studies of the humoral antibody response in rats of the random-bred Wistar strain, resistant to implantation of its "native" ascites tumor (AA), revealed a hemagglutinin that reacted with the erythrocytes of 90 per cent of Wistar strain rats.
The presence or absence of this hemagglutinogen (termed R-1 factor hemagglutinogen) in the host's tissues determined intraperitoneal AA tumor growth or rejection, respectively.
A second (weaker ?) histocompatibility factor was detected by subcutaneous implantation of AA ascites and appeared to be nonhemagglutinogenic.
Based upon a multiple allele hypothesis this study has indicated the existence of three alleles controlling the presence or absence of two possible histocompatibility antigens, R-1a (BC), R-1b (Bc), and R-1c (bc). The hemagglutinogen has been designated as B.
Several rat strains were screened for the R-1 hemagglutinogen (B). The inbred P.A. strain was 100 per cent R-1-positive, and the inbred Lewis strain was 100 per cent R-1-negative, indicating the homogeneity of inbred systems. Heterogeneity was indicated in the random-bred Wistar strain (90 per cent R-1 positive), and in the pen-bred Chocolate strain (88 per cent R-1-positive).
The anti-R-1 (anti-B) hemagglutinin appeared to be a "serum agglutinin" resembling the incomplete form of the human Rh antibody in that its avidity for the R-1-positive erythrocyte was markedly reduced in saline concentrations greater than that found normally in serum.
A cytotoxic antibody reactive against the R-1a AA tumor could be induced in R-1c rats by both normal and tumor tissues containing the R-1 hemagglutinogen.
The cytotoxic antibody in anti-R-1 sera was easily and completely absorbable by R-1-positive tumor cells but only partially by R-1-positive erythrocytes.
The parallelism between the activity of the R-1 antigens in the rat and the H-2 antigens in the mouse, and the relationship of the R-1 factor to certain blood groups in the rat, are discussed.
* This work was supported in part by a research grant from the National Cancer Institute of the National Institutes of Health, U.S. Public Health Service, and by a research grant from the Damon Runyon Fund, Inc.
Present address: Division of Cancer Immunology, The Biochemical Research Foundation, Newark, Delaware.
Received 4/24/60.
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