Publikationsdatum:
1995-11-17
Beschreibung:
Interferon gamma (IFN-gamma) responsiveness in certain cells depends on the state of cellular differentiation or activation. Here an in vitro developmental system was used to show that IFN-gamma produced during generation of the CD4+ T helper cell type 1 (TH1) subset extinguishes expression of the IFN-gamma receptor beta subunit, resulting in TH1 cells that are unresponsive to IFN-gamma. This beta chain loss also occurred in IFN-gamma-treated TH2 cells and thus represents a specific response of CD4+ T cells to IFN-gamma rather than a TH1-specific differentiation event. These results define a mechanism of cellular desensitization where a cytokine down-regulates expression of a receptor subunit required primarily for signaling and not ligand binding.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bach, E A -- Szabo, S J -- Dighe, A S -- Ashkenazi, A -- Aguet, M -- Murphy, K M -- Schreiber, R D -- New York, N.Y. -- Science. 1995 Nov 17;270(5239):1215-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Center for Immunology, Washington University School of Medicine, St. Louis, MO 63110, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7502050" target="_blank"〉PubMed〈/a〉
Schlagwort(e):
Animals
;
Antigens, CD/*biosynthesis
;
Cell Differentiation
;
Cell Line
;
Cytokines/biosynthesis
;
Down-Regulation
;
Gene Expression
;
Genes, MHC Class I
;
Interferon-gamma/*pharmacology
;
Ligands
;
Mice
;
Mice, Transgenic
;
Receptors, Interferon/*biosynthesis
;
Th1 Cells/cytology/immunology/*metabolism
;
Th2 Cells/cytology/immunology/*metabolism
Print ISSN:
0036-8075
Digitale ISSN:
1095-9203
Thema:
Biologie
,
Chemie und Pharmazie
,
Informatik
,
Medizin
,
Allgemeine Naturwissenschaft
,
Physik
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