Mahadev Patel - Academia.edu (original) (raw)

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Papers by Mahadev Patel

Cellular Immunology, 1990

Staphylococcal enterotoxin B (SEB) binds specifically to major histocompatibility complex class I... more Staphylococcal enterotoxin B (SEB) binds specifically to major histocompatibility complex class II molecules on the surface of accessory cells and stimulates virtually all T cells bearing certain, but not all, T cell-receptor VP alleles. We have previously shown that this superantigen is a potent inducer of multiple regulatory T cell populations. In the present report we show that SEB induces a population of suppressor T cells which inhibits the generation of alloantigeninduced cytotoxic T cell activity. Using both negative-and positive-selection analysis, we found that this suppressor population is a CD4-CD8-CD5+ IL-2R+ T cell. This cell population inhibited both syngeneic and allogeneic cytotoxic T lymphocyte activity, but the cell population which inhibited allogeneic CTL activity was radiation sensitive. In addition, allogeneic SEB-primed cells appeared to develop cytolytic activity as a result of the additional stimulation in the mixedlymphocyte reaction culture. The relationship of the SEB-primed CD4-CD8-CD5+ T cells to related regulatory T cell populations is discussed. o 1990 Academic press, hc.

Mechanisms of Cytotoxicity by NK Cells, 1985

Cellular Immunology, 1986

We have previously shown that staphylococcal enterotoxin B (SEB) is a potent inducer of suppresso... more We have previously shown that staphylococcal enterotoxin B (SEB) is a potent inducer of suppressor T cells which function to inhibit antibody production in vitro. In the present paper we extend these studies and show that the SEB-induced suppressor cells also inhibit the development of cytotoxic lymphocytes in mixed-lymphocyte reaction (MLR) cultures. Since further analysis also showed that the level of interleukin 2 (IL-2) in cultures of SEB-primed cells was significantly reduced, experiments were carried out to determine the role of IL-2 in the inhibition of cytotoxic cell activity. Attempts to neutralize the suppression by supplementing MLR cocultures with delectinated supernatants from concanavalin A (Con A)-stimulated rat splenocytes were not successful. In addition, MLR cocultures supplemented on Day 0 with 50 units of affinity-purified IL-2 were also suppressed. Further analysis showed that the IL-2 activity in the supplemented MLR cocultures containing suppressor cells were significantly reduced by Day 3. However, repeated supplementation of the MLR cocultures with exogenous IL-2 was successful in achieving (and maintaining) "normal" levels of IL-2. The cytotoxic cell activity in these MLR cocultures remained suppressed. These results suggest that the inhibition of cytotoxic cell activity by SEB-induced suppressor cells is independent of IL-2 levels in the MLR coculture.

Journal of Clinical Immunology, 1983

Analysis of peripheral blood leukocytes from a patient with angioimmunoblastic lymphadenopathy us... more Analysis of peripheral blood leukocytes from a patient with angioimmunoblastic lymphadenopathy using monoclonal antibodies and the fluorescence-activated cell sorter showed an unusually high proportion of cells that were OKT10+OKM1+63D3−. Since a large proportion of the large granular lymphocytes associated with natural killing in humans bears this surface phenotype, both blood and lymph node cells were subsequently tested for cell-mediated cytotoxicity in natural killer (NK)-cell assays. Following chemotherapy, both cells bearing the NK surface phenotype and the NK cytotoxicity disappeared and a population of cells, bearing none of the typical lymphocyte or monocyte markers, became dominant. At this point the patient was diagnosed as having immunoblastic sarcoma and shortly thereafter succumbed to his disease. In the few cases where extremely high levels of NK activity have been reported, the tumor cells themselves have been responsible for cell-mediated cytotoxicity. In this case, the final tumor population had no NK activity. Thus either a subpopulation of cytotoxic tumor cells was destroyed by chemotherapy or the patient had expanded numbers of NK cells reacting against his tumor prior to therapy.