       Document 0296
 DOCN  M9630296
 TI    Ligand-induced autoregulation of IFN-gamma receptor beta chain
       expression in T helper cell subsets.
 DT    9603
 AU    Bach EA; Szabo SJ; Dighe AS; Ashkenazi A; Aguet M; Murphy KM; Schreiber
       RD; Center for Immunology, Washington University School of Medicine,;
       St. Louis, MO 63110, USA.
 SO    Science. 1995 Nov 17;270(5239):1215-8. Unique Identifier : AIDSLINE
       MED/96072977
 AB    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.
 DE    Animal  Antigens, CD/*BIOSYNTHESIS  Cell Differentiation  Cell Line
       Cytokines/BIOSYNTHESIS  Down-Regulation (Physiology)  Gene Expression
       Genes, MHC Class I  Interferon Type II/*PHARMACOLOGY  Ligands  Mice
       Mice, Transgenic  Receptors, Interferon/*BIOSYNTHESIS  Th1
       Cells/CYTOLOGY/IMMUNOLOGY/*METABOLISM  Th2
       Cells/CYTOLOGY/IMMUNOLOGY/*METABOLISM  JOURNAL ARTICLE

       SOURCE: National Library of Medicine.  NOTICE: This material may be
       protected by Copyright Law (Title 17, U.S.Code).

