Origin of mink cytopathic focus-forming (MCF) viruses:comparison with ecotropic and xenotropic murine leukemia virus genomes.
Explore the source record for details and available documents.
Biomedical subjects
Publications and source records attributed to S Gupta.
Explore the source record for details and available documents.
In autologous mixed lymphocyte reaction (MLR), T cells proliferate in response to the stimulation by autologous non-T cells. In the present study, human T cell subpopulations, defined by murine monoclonal antibodies OKT4, OKT8, or 9.3, were examined for their capacity to proliferate in autologous and allogeneic MLR. It was observed that the treatment of responder T cells with OKT4 or 9.3 antibody (both defining helper/inducer T cells) and complement (C') ablated their proliferative response in autologous MLR and markedly reduced their allogeneic MLR proliferative response. In contrast, treatment of T cells with OKT8 antibody (defining suppressor/cytotoxic T cells) and C' had no or minimal effect on their proliferative response in autologous MLR. Furthermore, OKT4, 9.3, 9.6 (PAN), or 7.2 anti-human Ia (framework specific) but OKT8 antibody, when present during the entire culture period, in the absence of C' inhibited in a dose-dependent manner the proliferative response in both autologous and allogeneic MLR. Inhibition of proliferation was also observed when the responder T cells were pretreated with OKT4 or 9.3 antibody, washed, and then stimulated with irradiated autologous or allogeneic non-T cells. Pretreatment of T cells with OKT8 or 7.2 anti-Ia antibody in the absence of C' did not influence their proliferative response in autologous MLR. Thus, T cells containing cells with helper/inducer activity defined by OKT4 or 9.3 antibody appear to be the major responder T-cell subpopulation in autologous MLR.
Human peripheral blood T lymphocytes were separated into theophylline-resistant (TR) and -sensitive (TS) subpopulations. Proliferative responses TR, TS and unfractionated T cells were studied, using irradiated autologous or allogeneic non-T cells as stimulators. TR cells proliferated vigorously in both autologous and allogeneic mixed lymphocyte cultures (MLC). TS cells. which constitute about 20% of unfractionated T cells, exhibited poor proliferative responses to autologous and allogeneic stimulation. The magnitude of proliferation in autologous and in allogeneic MLC was found to be directly dependent on the number of TR cells in the culture. Mitomycin-C (MMC)-treated TR cells augmented and MMC-treated TS cells suppressed (P less than 0.05) the autologous and allogeneic MLC responses of unfractionated T cells. However, the response of TS cells did not increase in autologous or allogeneic MLC when co-cultured with MMC-treated TR cells. MMC-treated TS cells, when co-cultured with TR cells, suppressed the responses of TR cells (P less than 0.05). The enhancing effect of TR cells was radiation-resistant. Suppressor influence of TS cells, in contrast, was abolished by irradiation (P less than 0.05). These findings demonstrate that TR cells are the responding cell in autologous MLR and augment the MLC responses of unfractionated T cells. TS cells, on the other hand, respond poorly in autologous or allogeneic MLC and suppress the response of TR cells.
Explore the source record for details and available documents.
Two cases of middle aortic syndrome in children are described along with two other cases reported earlier. In childhood, this disease may present as incipient or overt cardiac failure. Surgical treatment should be undertaken based on an objective assessment of the severity of the stricture and after taking into account the future growth of the child.
Explore the source record for details and available documents.
Peripheral blood from 4 patients with progeria and their family members and 2 patients with Werner's syndrome were analyzed for the proportion of total T cells and T cells with receptors for IgM (Tmu) or IgG (Tgamma). In 3 patients proportions of Tmu cells were within the range for age- and sex-matched controls. 1 patient had significantly lower proportions of Tmu cells when compared to age- and sex-matched controls. The proportions of Tgamma cells were increased in 2 and were within the range for normal controls in the remaining 2 patients. When data were analyzed with regard to Tmu/Tgamma ratios, 3 of 4 patients exhibited ratios lower than the lowest limit observed in age- and sex-matched controls. Surprisingly, family members in all four families exhibited patterns of Tmu and Tgamma cells similar to that seen in the patient. Both patients with Werner's syndrome had proportions of Tgamma cells, resulting in low Tmu/Tgamma ratios.
Forty-five patients with Takayasu's disease were studied between 1972 and the end of 1979. Operative treatment was less frequently needed for aortic arch disease than for descending aorta disease. Correct evaluation may be difficult in the latter till the time of operative exploration. Children with significant stenosis need early operation and a "plasty' type of repair is favoured over bypass grafts. Contrary to some descriptions, the disease process can affect the region of the aortoiliac bifurcation, needing surgical management based on established principles. Correct evaluation can make operative treatment safe and rewarding for those patients who need intervention as the recurrence rate of the disease process has been low in surgically treated patients. Immunologically the patients show defective T-lymphocyte function, increase in ther serum level of IgG, and a reduction in serum complement constituents C3 and C4, indicating the possibility of formation of a complement-binding immune complex. Histochemical studies show deposition of IgG and PAS-positive material in the intima and probable deposition of IgM and IgA in the junctional area of media and intima, with total destruction of the elastic lamina. A hypothesis for the pathogenesis of the disease is presented.
Explore the source record for details and available documents.
Almost every T cell-mediated immune defect has been observed in patients with Hodgkin's disease. These immune defects are present as early as Stage I disease. T cell-mediated immune defects appears to be due to both cellular and serum factors. The demonstrable immune defects found in family members, including spouses, suggest a horizontal transmission of disease, perhaps by a virus. However, these family studies remain to be confirmed and extended to twins who do not live together.
Explore the source record for details and available documents.
Optimal conditions were established for evaluating the phytohemagglutinin-induced proliferative responses of purified peripheral blood T lymphocytes. This assay was utilized to determine whether T cells (in the absence of monocytes and serum inhibitory factors) from patients with Hodgkin's disease were defective in their ability to proliferative in response to optimal (50 microgram/ml) and suboptimal (25 and 12.5 microgram/ml) concentrations of phytohemagglutinin. T cells from 6 of 12 untreated patients exhibited 6-day proliferative responses below the range of 15 control subjects using optimal mitogen concentrations, and 9 of 12 patients exhibited subnormal responses using lower concentrations. Kinetic analyses indicated that the abnormal T-cell proliferative responses were characterized by peak proliferation occurring at day 4 or 5, rather than day 6. The observed abnormalities were not related to elevations in the proportions of T cells bearing surface receptors for IgG (T gamma Cells). Our results suggest that intrinsic functional T-cell defects contribute to the impaired immunity associated with Hodgkin's disease.
The proliferative response to peripheral blood mononuclear cells to phytohemagglutinin was enhanced at 40 degrees C when compared to those at 37 degrees C. This change in proliferative response was not affected by depletion of macrophages. However, T and non-T subsets of lymphocytes, separated by sheep red-blood cell rosetting technique, differed in their responsiveness to mitogens at elevated temperatures. The replication of DNA in T cell by phytohemagglutinin was enhanced at 40 degrees C. The kinetics of proliferative response with regard to dose of mitogen or duration of culture was similar at both temperatures. The response of non-T cells (B-cell enriched fraction) to pokeweed mitogen was unaffected. Similar result were obtained in experiments with lymphocytes from tonsil and thymus. Coculture of purified T and non-T cells from the same individual showed that responses to mitogens were synergistically stimulated both at 37 and 40 degrees C. The effect of elevated temperatures on the response of lymphocytes to concanavalin A was found to be variable.
Four of 18 patients with common variable immunodeficiency and one of eight patients with selective IgA deficiency had increased proportions of T epsilon cells. Three patients with common variable immunodeficiency and two with selective IgA deficiency had increased numbers of T epsilon cells. Three patients with common variable immunodeficiency had decreased numbers of T epsilon cells. Five of six patients with hyperimmunoglobulinaemia E had high proportions of T epsilon cells; this increase was not related to the elevated IgE levels.
Subpopulations of lymphocytes in the peripheral blood and spleen from adult untreated patients with Hodgkin's disease were studied for spontaneous (SCMC) and antibody-dependent cellular cytotoxicities (ADCC). Peripheral blood from seven of 24 patients demonstrated abnormally low T cell-mediated SCMC when compared to age- and sex-matched healthy controls. Only two of these patients also demonstrated low T cell ADCC and non-T cell-mediated SCMC and ADCC. T cell ADCC in the peripheral blood of patients with involved spleen was significantly higher (P less than 0.05) when compared to those in whom spleen was not involved. When SCMC and ADCC were compared between peripheral blood and splenic lymphocytes with regard to involvement of spleen by Hodgkin's disease, non-T cell SCMC in the involved spleen was significantly lower (P less than 0.05) than their peripheral blood non-T cell SCMC. SCMC and ADCC tended to be higher in patients with stages III and IV of Hodgkin's disease when compared to those with stages I and II. However, the differences were not statistically significant. No direct relationship was observed between T and SCMC or ADCC and the proportion of T cells with IgG Fc receptors (T gamma). The significance of these observations is discussed.
The effect of a single dose (300 mg) of intravenous hydrocortisone on T cell colony and cluster formation was examined in healthy normal volunteers. Peripheral venous blood was drawn before and 4 and 24 hr following administration of the drug T cell colonies (greater than 50 cells/aggregate) and clusters (10-50 cells/aggregate) in response to PHA were assayed by one-stage stimulation in the microagar culture using glass capillaries. The maximum numbers of colonies and clusters were observed between days 7 and 8 of culture. At 4 hr following administration of the drug, both colony and cluster counts were significantly reduced (P less than 0.01). Colony and cluster counts returned to the initial levels 24 hr following administration of the drug. These changes in T cell clusters and colonies were accompanied with changes in the proportions of T cells with IgM (T micro) and IgG (T gamma) receptors. This study demonstrates that a single dose of i.v. hydrocortisone depresses T cell clonal expansion and suggests that this effect could be secondary to the redistribution of a subpopulation of T cells among peripheral blood and other lymphoid tissues and is perhaps not due to a direct suppression of the proliferative response. The significance of these observations is discussed.
Explore the source record for details and available documents.