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S E Dorsch

Publications and source records attributed to S E Dorsch.

35 records · Page 2Linked to original sources
PubMed1984

Suppressor T cells in rats with prolonged cardiac allograft survival after treatment with cyclosporine.

DA rats treated with cyclosporine for 2 weeks after being grafted with an RT1-incompatible PVG heart graft did not reject the graft and developed a state of specific unresponsiveness to graft antigens. The cellular mechanisms maintaining this state of unresponsiveness were studied by testing the capacity of lymphocytes from these animals to effect or inhibit graft rejection in irradiated grafted hosts. Whole lymph node and spleen cell populations, and the T cell subpopulation separated from the latter, failed to restore the rejection of PVG hearts in irradiated DA recipients but restored third-party Wistar-Furth (W/F) rejection. Both whole spleen cells and the splenic T cell subpopulation had the capacity to suppress the ability of normal DA lymphocytes to cause graft rejection. Suppression was not dependent upon a state of chimerism in grafted cyclosporine -treated animals, and was not associated with any measurable alterations in the proportion of cytotoxic/suppressor T cells in lymphoid tissues. These studies show that the state of specific unresponsiveness that follows the treatment of heart grafted rats with cyclosporine is dependent, in part, upon active suppression that is induced or mediated by T lymphocytes. Many features of the immune reactivity of cyclosporine -treated grafted rats support the hypothesis that the mechanism of specific suppression in these animals is akin to that of enhancement, rather than to that of transplantation tolerance induced in neonatal rats.

Animals↗
PubMed1984

Lymphocyte subsets in Heymann nephritis.

Altered ratios of T lymphocyte subsets have recently been reported in some forms of glomerulonephritis, including membranous glomerulonephritis. Heymann nephritis is a model of membranous glomerulonephritis that can be induced in susceptible strains of rat by a single subcutaneous injection of renal tubular antigen in Freund's complete adjuvant. Monoclonal antibodies were used to identify cytotoxic/suppressor and helper/inducer T cells in the blood, spleen, peripheral lymph nodes, and, where relevant, the lymph node draining the antigen injection site in susceptible and nonsusceptible rat strains before and after immunization with renal tubular antigen. A marked interstrain variation in the proportions of T lymphocyte subsets was found, but this did not segregate strains that are susceptible to Heymann nephritis induction from those that are resistant. Neither the development of Heymann nephritis in susceptible strains or immunization of resistant strains with renal tubular antigen was associated with any specific alteration in the T lymphocyte subpopulations.

Animals↗
PubMed1983

Neoplasia in adoptively immunosuppressed rats. A possible model for tumorigenesis in transplant recipients.

An extremely high incidence of malignant tumors was observed in groups of rats that had previously been exposed to whole body irradiation, grafted with allogeneic tissue, and injected with lymphocytes capable of specifically suppressing the rejection of the grafted tissue. Neoplasia in these adoptively immunosuppressed rats had features in common with that in therapeutically immunosuppressed transplant recipients. Increased tumor incidence could not be accounted for on the basis of the effects of whole body irradiation or failure of immune surveillance, nor could it be a direct effect of lymphoid tissue stimulation. It is suggested that cell mediated suppressor responses play a critical role in tumorigenesis. The mechanism of this is not simply direct stimulation of lymphoid tissue proliferation.

Animals↗
PubMed1983

The cellular basis of allograft rejection in vivo. III. Restoration of first-set rejection of heart grafts by T helper cells in irradiated rats.

An adoptive transfer model was used to examine the subpopulations of lymphocytes required to effect first-set rejection of directly vascularized heart allografts. PVG heart grafts are not rejected in irradiated DA hosts for at least 50 days. The adoptive transfer of 5 X 10(7) syngeneic lymph node cells (LNC) restores rejection to 14.4 +/- 2.4 days (mean +/- SD). Subpopulations of LNC, were separated by an indirect "panning" technique using the mouse antirat monoclonal antibodies W3/13, MRC OX8, or W3/25 to deplete the unwanted subsets of cells. Each subpopulation was tested, in a number equivalent to the number present in 5 X 10(7) normal LNC, for its ability to cause the rejection of heart grafts. Whole T cells (W3/13+) or helper/inducer T cells (W3/25+) restored graft rejection to 16.4 +/- 3.8 d and 16.0 +/- 2.4 days, respectively. Neither cytotoxic/suppressor T cells (MRC OX8+) nor B cells (Ig+) restored rejection. Indirect immunoperoxidase stains of the grafts showed that although W3/25+ cells predominated in the rejected tissue, MRC OX8+ cells were also present even in grafts from rats restored with inocula that contained less than 1% MRC OX8+ cells. Examination of lymphoid tissues suggested that the MRC OX8+ cells might be of host origin. By the time the grafts were rejected in irradiated hosts, significant thymic regeneration had occurred and there were large numbers of MRC OX8+ cells present in the thymus, as well as some in lymph nodes and spleen.

Animals↗
PubMed1976

T cell leukaemia in the rat: stable marker chromosome in leukaemic cells.

The karyotype of a transplantable T cell leukaemia which arose originally in a PVG strain rat undergoing chronic internal beta irradiation of the spleen was examined and a marker chromosome was found. Although the leukaemia progressively became more acute during 4 years of continuous passage the marker did not change. Cytogenetic analysis of normal rats given an acute exposure to external irradiation revealed, among other abnormalities, a marked of the same morphology indicating that the original marker was probably radiation induced. This is the first description of a stable marker chromosome in an experimental animal leukaemia.

Animals↗
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