home
***
CD-ROM
|
disk
|
FTP
|
other
***
search
/
The Arsenal Files 6
/
The Arsenal Files 6 (Arsenal Computer).ISO
/
health
/
med9603.zip
/
M9630296.TXT
< prev
next >
Wrap
Text File
|
1996-02-27
|
2KB
|
32 lines
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).