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Biomedical subjects

D S Nelson

Publications and source records attributed to D S Nelson.

At least 109 records · Page 6Linked to original sources
PubMed1978

Effect of hydrocortisone on the response of rat lymphocytes to phytohaemagglutinin.

The proliferative response of rat peripheral blood lymphocytes and spleen cells to phytohaemagglutinin (PHA) was studied following treatment with single or multiple doses of hydrocortisone. A transient lymphopaenia with a rapid recovery at 24 h occurred with both dose schedules. Hydrocortisone in vitro caused a dose-dependent depression of blood lymphocyte response to PHA but enhanced the response of spleen cells when the steroid was added after the mitogen. An inverse relationship between blood and splenic lymphocyte responses to PHA occurred after a single dose of hydrocortisone. Blood lymphocytes from multiple dose hydrocortisone-treated rats had an enhanced response to PHA. Serum collected within 5 min of injection from single dose-treated rats depressed normal rat blood lymphocyte responses. After multiple doses of hydrocortisone serum enhanced blood lymphocyte responses to PHA. The primary antibody response to sheep erythrocytes was only affected by near toxic doses of hydrocortisone.

Animals↗
PubMed1978

Immune reactions in human filariasis.

Sera from cases of elephantiasis due to Wuchereria bancrofti infection promoted an intense adhesion of peripheral blood leukocytes to W. bancrofti microfilariae in vitro. A similar adhesion was also seen using sera from some normal persons living for several years in areas where filariasis is endemic. No such adhesion was evident with sera from microfilaria carriers or from normal subjects from nonendemic areas. The adhesion was complement independent and was associated with the immunoglobulin G fraction of serum. 51Cr release studies suggested the occurrence of cell-mediated cytotoxicity to W. bancrofti microfilariae in the presence of elephantiasis serum. Microfilariae of Litomosoides carinii could be isolated free of blood cells, from the blood of infected rats. In the presence of serum, or its immunoglobulin G fraction, from patients with elephantiasis, L. carinii microfilariae adhered to human peripheral blood leukocytes or rat spleen cells.

Animals↗
PubMed1978

Macrophages and resistance to tumours: influence of agents affecting macrophages and delayed-type hypersensitivity on resistance to tumours inducing concomitant immunity.

Early, specific concomitant immunity to each of four tumours was inhibited by treatment with silica or carrageenan. Late, non-specific concomitant immunity was, with one exception, not inhibited by these agents. Treatment of non-immune mice with silica at certain critical periods before challenge promoted the growth of four of six syngeneic methylcholanthrene-induced tumours in their feet. Treatment with carrageenan was much less effective. Early and late concomitant immunity were inhibited by one or more agents inhibiting delayed-type hypersensitivity: irradiation, niridazole and reserpine. Irradiation of non-immune mice did not effect the growth of tumours in their feet. Treatment of non-immune mice with niridazole or reserpine actually inhibited the growth of some tumours. It is suggested that (a) mice offer some natural resistance to tumour growth, macrophages perhaps being effectors; (b) some tumour isografts may survive only if an inflammatory reaction occurs; (c) mechanisms akin to those of delayed-type hypersensitivity operate in the expression of concomitant immunity; (d) macrophages are important in early, specific concomitant immunity, but perhaps less so in the late non-specific phase.

Animals↗
PubMed1977

Autoantibodies in cancer patients.

The prevalence of antinuclear antibodies was increased in patients with adenocarcinoma of the corpus uteri, chronic lesions of the cervix uteri, malignant melanoma, non-malignant pigmented skin lesions and basal cell carcinoma. The prevalence of smooth muscle antibodies was increased in patients with squamous carcinoma of the cervix and malignant melanoma. The prevalence of antibodies to gastric parietal cells and thyroid epithelial cells was not increased in any group of patients.

Adenocarcinoma↗
PubMed1976

Effect of sera from immunologically altered mice on phytohemagglutinin-induced mouse lymphocyte transformation.

The DNA-synthetic response of mouse spleen cells to phytohemagglutinin in vitro is depressed by the addition of normal mouse serum. The effects of sera from mice that had been modified immunologically were examined. Increased depressive activity was found in sera from nude mice and from mice recently treated with anti-thymocyte globulin, but no change was found in sera from thymectomized, irradiated, bone marrow-reconstituted mice, nor from lethally or sublethally irradiated or cyclophosphamide-treated mice. Base line DNA synthesis was, however, less inhibited by sera from irradiated or cyclophosphamide-treated mice. Increased depressive activity was found in sera from mice with graft-versus-host reaction and from mice injected with Salmonella enteritidis 11RX, in which macrophage stimulation occurred. Increased depressive activity was also found in the sera of mice injected with sheep erythrocytes. T cells do not appear to be a source of depressive activity but B cells, macrophages and nonlymphoid cells may be sources.

Animals↗
PubMed1976

Macrophages and lymphoid tissues in mice with concomitant tumour immunity.

The growth in mice of subcutaneous isografts of any of 5 methylcholanthrene-induced fibrosarcomas was associated with macrophage stimulation, reflected in an increased incidence of DNA-synthesizing cells among marcophages in the uninjected peritoneal cavity. This occurred at some stage with 4 tumours that induced concomitant immunity and one that did not. Some degree of splenomegaly also occurred with all 5 tumours. The spleens of all the tumour-bearing mice showed histological evidence of increased haemopoietic activity. Histological changes in the lymphoid elements of the spleen were very different with different tumours, ranging from lymphoid stimulation to lymphoid atrophy. The lymph nodes draining the sites of primary isografts which induced concomitant immunity showed signs of stimulation in the paracortical areas, followed by plasmacytopoiesis in the medullary areas. Stimulation of the paracortical areas was not detected in the nodes draining sites of injection of a tumour not inducing concomitant immunity. Nodes draining the sites of challenge isografts in mice exhibiting concomitant immunity showed plasmacytopiesis.

Animals↗
PubMed1975

Specificity of cell-mediated cytotoxicity against human melanoma lines: evidence for "non-specific" killing by activated T-cells.

The specificity of cell-mediated cytotoxicity against melanoma cells in vitro has been analyzed in a large number of studies with cells both from normal and melanoma subjects. As in a number of other, recent, similar human studies, no evidence for tumour specificity was found. Effector cells in peripheral blood responsible for the cytotoxic raction were examined by cell separation methods based on red cell rosette formation and separation through Hypaque-Ficoll mixtures. The evidence suggests that non-specificity results from killing by cells separating largely in the non-sheep red blood cell rosetting fraction and which have cytotoxic specificity directed broadly to cells with abnormal membranes. Further analysis revealed that the cells were non-phagocytic and did not bear receptors for complement. They appear to be activated into cell division and to bear surface receptors for the Fc portion of IgG. Additional evidence is presented suggesting that the cells mainly responsible are activated thymus-dependent cells present in the circulation of both tumour-bearing and normal subjects.

Antigen-Antibody Reactions↗
PubMed1975

Cellular basis for the immune response to methylcholanthrene-induced tumors in mice. Heterogeneity of effector cells.

Immune resistance to methylcholanthrene-induced tumors has two phases, an early specific and a late non-specific phase. Both phases were found to be T-cell-dependent in vivo. Thus, adult thymectomized, irradiated, bone-marrow-protected mice bearing H-1 tumor isografts showed impaired resistance to challenge with homologous (H-1) and heterologous (H-3) tumor cells. In each case resistance was restored by injection of thymus cells. In vitro analysis of the cellular basis of resistance revealed that different mechanisms were involved in the two phases. The cytotoxic effect of immune spleen cells taken during the early specific phase was inhibited by pretreatment with anti-O serum and complement and by removal of macrophages. Neither procedure, however, interfered with the cytotoxic potential of immune spleen cells taken during the late non-specific phage of immunity. Passage of immune spleen cells through rabbit-IgG anti-mouse immunoglobulin-coated columns (which yielded a T-cell-enriched, B-cell-depleted population) resulted in abrogration of cytotoxicity whether the cells were obtained during the early or the late phase of resistance. The inability of late-phase spleen cells to kill was explicable in terms of B-cell removal since T-cells and macrophages had been shown to be ineffective at that time. In contrast, the failure of column-treated cells from the early phase to kill was found to be due to removal of adherent cells rather than B-cells since cytotoxicity (1) was abrogated by passage through control columns coated with rabbit-IgG anti-sheep red blood cell antibody which did not retain B-cells and (2) could be restored by addition of immune macrophages (from anti-O serum-treated spleens). Taken together, these results indicate that the cellular basis of immune resistance to methylcholanthrene-induced tumors is heterogeneous. The early specific phase seems to be mediated by an interaction between T-cells and macrophages; the late none-specific phase, although T-cell dependent in its induction, depends on a different effector mechanism, possibly involving a cell or its products of the B lineage.

Animals↗