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  Antigen-Dependent Release of IFN-γ by Cytotoxic T Cells Up- Regulates Fas on Target Cells and Facilitates Exocytosis- Independent Specific Target Cell Lysis

Müllbacher, A., Lobigs, M., Hla, R. T., Tran, T., Stehle, T., & Simon, M. M. (2002). Antigen-Dependent Release of IFN-γ by Cytotoxic T Cells Up- Regulates Fas on Target Cells and Facilitates Exocytosis- Independent Specific Target Cell Lysis. Journal of Immunology, 169(1), 145-150.

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 Urheber:
Müllbacher, Arno, Autor
Lobigs, Mario, Autor
Hla, Ron T., Autor
Tran, Thao1, Autor           
Stehle, Thomas2, Autor           
Simon, Markus M.2, Autor           
Affiliations:
1Department of Cellular Immunology, Max Planck Institute of Immunobiology and Epigenetics, Max Planck Society, ou_2243657              
2Metchnikoff Laboratory, Max Planck Institute of Immunobiology and Epigenetics, Max Planck Society, ou_2243654              

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 Zusammenfassung: Effector cytolytic T (Tc) lymphocytes, deficient in the exocytosis-mediated pathway of target cell lysis, induce Fas on target cells and, in turn, delayed cell death and apoptosis via the Fas ligand-Fas interaction. The induction of Fas can be blocked by anti IFN-γ Abs. This Fas up-regulation on initially Fas-negative target cells is not mediated by TCR-MHC/peptide signaling per se, but by secreted IFN-γ from Tc cells after Ag engagement. The Fas up-regulation by Tc cells can be mimicked by treatment of target cells with rIFN-γ. Tc cells from IFN-γ knockout mice do not induce Fas expression on target cells. Te cell-mediated Fas expression on third party, bystander, target cells does not enhance their susceptibility to lysis by these nominal effector cells. The results are discussed as to the possible relevance of the phenomenon in efficiency and regulation of the Tc cell response to infections by viruses.

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Sprache(n): eng - English
 Datum: 2002-07-01
 Publikationsstatus: Erschienen
 Seiten: -
 Ort, Verlag, Ausgabe: -
 Inhaltsverzeichnis: -
 Art der Begutachtung: Expertenbegutachtung
 Identifikatoren: eDoc: 20953
ISI: 000176360400020
 Art des Abschluß: -

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Titel: Journal of Immunology
  Alternativer Titel : J. Immunol.
Genre der Quelle: Zeitschrift
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Ort, Verlag, Ausgabe: -
Seiten: - Band / Heft: 169 (1) Artikelnummer: - Start- / Endseite: 145 - 150 Identifikator: ISSN: 0022-1767