Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P14784 (IL-2 receptor)
 3,849 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Human T lymphocyte proliferation induced by neuraminidase-galactose oxidase (NAGO)-treated autologous erythrocytes (HENAGO) plus polyethylene glycol (PEG) has previously been shown to be independent of accessory cells. Here, we show that the response to HENAGO + PEG was accompanied by interleukin 2 (IL-2) release and was inhibited by anti-IL-2 and anti-IL-2 receptor antibodies. HENAGO alone initiated DNA synthesis together with phorbol ester (12-O-tetradecanoyl-phorbol-13-acetate; TPA). To elucidate the nature of the stimulatory signals NAGO-treated sheep erythrocytes (SENAGO) were used in additional experiments. In parallel to the superior rosetting capacity of SE compared to HE. SENAGO were by themselves stimulatory, and the response was further enhanced by PEG or TPA. Antibody L180/1, specific for the T11 (CD2) target structure (T11TS) on SE, homologous to the human CD2 ligand LFA-3, abolished the response to SENAGO alone or when combined with PEG or TPA. The results suggest that ENAGO induce T-cell response through CD2-LFA-3-T11TS interaction, and via other surface antigens bound by the oxidatively induced aldehyde groups on ENAGO.
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PMID:Activation of human T cells by neuraminidase-galactose oxidase-treated erythrocytes involving CD2 (T11) and its complementary structure. 289 54

Human thymocytes were separated by peanut agglutinin (PNA) into PNA+ and PNA- cell fractions, and directly oxidized by the combined action of the enzymes neuraminidase and galactose oxidase (NAGO). Such treatment resulted in the induction of interleukin 2 (IL-2) responsiveness in PNA- cells but not in PNA+ cells. The molecular basis for the poor IL-2 responsiveness of PNA+ cells resides in their inability to express sufficient amounts of IL-2 receptors in response to NAGO treatment. Irradiated oxidized PNA+ or PNA- cells are able to transmit an oxidative mitogenic signal to autologous native PNA- cells but not to PNA+ cells. Depletion of plastic adherent cells from the PNA+ subpopulation totally abolished its high potency for the indirect signal transduction, whereas accessory cell depleted PNA- cells were affected to a lesser extent. Nonspecific esterase staining indicated that human thymic macrophages/monocytes are PNA+ cells. In spite of their small number (less than 0.5% of the total thymus cells) they appear to be very active in the indirect oxidative signal transmission. Unlike the indirect system, direct oxidative mitogenesis is independent of accessory cells. Attempts to detect NAGO-dependent IL-2 receptor inducing soluble factors were fruitless and there is a strict need for cell-cell interaction for the indirect transmission of the oxidative mitogenic signal.
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PMID:Cellular and growth factor requirements for the direct and indirect oxidative induction of interleukin 2 responsiveness in human thymocytes. 392 57