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W R Duncan

Publications and source records attributed to W R Duncan.

At least 55 records · Page 3Linked to original sources
PubMed1978

Analysis of the major histocompatibility complex in Syrian hamsters. II. Linkage studies.

The genetic control of the histocompatibility antigens that induce strong alloreactions in Syrian hamsters was examined. Genetic studies revealed that the alloantigens involved in skin graft rejection, graft-versus-host reactions, and mixed lymphocyte reactions are under dominant single gene control and that these genetic loci are closely linked. These data suggest that this strong histocompatibility locus (i) may represent the major histocompatibility complex equivalent in this species, and this locus or group of loci has been called Hm-1. In addition, studies concerning the genetic control of the immune response to bovine serum albumin suggest that the high response is under dominant, single gene control; however, this gene is not linked to Hm-1.

Animals↗
PubMed1978

Analysis of the major histocompatibility complex in Syrian hamsters. I. Skin graft rejection, graft-versus-host reactions, mixed lymphocyte reactions, and immune response genes in inbred strains.

Five inbred strains of Syrian hamsters (Mesocricetus auratus) were examined for the presence of disparity at a genetic region similar to the major histocompatibility complex in other species. Vigorous reciprocal alloreactions developed in several strain combinations, which resulted in acute skin graft rejection, strong mixed lymphocyte reactions, and potent graft-versus-host reactions. In addition, we found evidence for an immune response gene which controls the antibody response to bovine serum albumin. Patterns of alloreactivity observed for skin graft rejection, graft-versus-host reactivity, and mixed lymphocyte reactivity are compatible with the hypothesis that hamsters possess a major histocompatibility complex, but the absence of discernable disparity at a serologically defined locus makes a definitive statement premature.

Animals↗
PubMed1977

Analysis of the major histocompatibility complex in Syrian hamsters. III. Cellular and humoral immunity to alloantigens.

Among the genetic loci incorporated into the major histocompatibility complex in every species studied to date have been prominent genes encoding for strong histocompatibility determinants that elicit detectable alloantibody responses and which are the chief antigenic targets of cell-mediated cytotoxicity reactions. The K and D regions of the H-2 complex in the mouse and the A, B, and C regions of the HLA complex in man are representative examples. Syrian hamsters, as described in this report, do not make alloantibodies to antigens of this type and only very poorly do they carry out in vitro cell-mediated cytotoxicity to target cells putatively bearing these antigens. Since hamsters are quite capable of discriminating analogous antigenic differences in xenogeneic species, and xenogeneic sources cannot distinguish immunologically between the antigens encoded by the two hamster major histocompatibility alleles. Hm-1a and Hm-1b, we conclude that the hamster strains we work with are serologically indistinguishable by the methods used here. However, they obviously differ for determinants which elicit T cell-mediated responses, as evidenced by their ability to express acute skin graft rejection, mixed lymphocyte reactivity, graft-vs-host reactions, and cell-mediated cytotoxicity reactions. Such alloreactivity may reflect a mutation at an SD locus, affecting antigenic sites recognized only by T cells, or that the available hamster strains are SD identical, but differ at loci similar to the I region loci in mice. Alternatively, we cannot exclude the possibility that Syrian hamsters somehow fail to express properly the genes coding for SD determinants.

Animals↗
PubMed1975

Studies on the specificity of autoantibodies produced in systemic graft-vs-host disease.

Anti-erythrocyte antibodies were found in serum and on RBC of F-1 hybrid hamsters afflicted with systemic graft-vs-host (GVH) disease. These antibodies were shown to be reactive with antigenic determinants unique to hamster erythrocytes compared to heterologous erythrocytes and to non-erythrocytic hamster tissues. They fulfilled the criteria for true autoantibodies by failing to discriminate strain specificities among the domestically maintained isogenic hamster lines that were tested. It is suggested that the excessive production of these antibodies results from the allogeneic effect by which donor T-lymphocytes attack host B lymphocytes and stimulate heretofore quiescent self-reactive clones. Moreover,it is proposed that these autoantibodies can function as enhancing antibodies and subvert continued progression of GVH disease. In this regard, they resemble antibodies directed at allogeneic transplantation antigens that have been shown to attenuate and abort GVH processes.

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