Publication Date:
1995-07-14
Description:
The ability of interferon gamma (IFN-gamma) to inhibit the proliferation of type 2 T helper cells (TH2), but not that of type 1 (TH1) cells, suggests that helper cell subsets might differ in their activation of the IFN-gamma signaling pathway. The IFN-gamma-inducible signal transducing factor (STF-IFN gamma) was activated in murine TH2 but not in TH1 cell clones, because in the latter the second chain of the IFN-gamma receptor (accessory factor 1 or IFN-gamma R beta) was absent. Thus, TH1 cells use receptor modification to prevent the activation of STF-IFN gamma and achieve an IFN-gamma-resistant state.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Pernis, A -- Gupta, S -- Gollob, K J -- Garfein, E -- Coffman, R L -- Schindler, C -- Rothman, P -- New York, N.Y. -- Science. 1995 Jul 14;269(5221):245-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medicine, College of Physicians and Surgeons, Columbia University, New York, NY 10032, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7618088" target="_blank"〉PubMed〈/a〉
Keywords:
Animals
;
Base Sequence
;
Clone Cells
;
DNA-Binding Proteins/genetics/metabolism
;
Down-Regulation
;
Gene Expression Regulation
;
Interferon Regulatory Factor-1
;
Interferon-gamma/pharmacology/*physiology
;
Interleukin-4/pharmacology
;
Janus Kinase 1
;
Janus Kinase 2
;
Mice
;
Molecular Sequence Data
;
Phosphoproteins/genetics
;
Protein-Tyrosine Kinases/metabolism
;
*Proto-Oncogene Proteins
;
Receptors, Interferon/*physiology
;
STAT1 Transcription Factor
;
*Signal Transduction
;
Th1 Cells/*immunology/metabolism
;
Th2 Cells/*immunology/metabolism
;
Trans-Activators/metabolism
Print ISSN:
0036-8075
Electronic ISSN:
1095-9203
Topics:
Biology
,
Chemistry and Pharmacology
,
Computer Science
,
Medicine
,
Natural Sciences in General
,
Physics
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