The role of interferon γ in regulation of CD4+ T-cells and its clinical implications

Chen, Jiezhong and Liu, Xiaosong (2009) The role of interferon γ in regulation of CD4+ T-cells and its clinical implications. Cellular Immunology, 254 2: 85-90. doi:10.1016/j.cellimm.2008.09.001


Author Chen, Jiezhong
Liu, Xiaosong
Title The role of interferon γ in regulation of CD4+ T-cells and its clinical implications
Formatted title
The role of interferon γ in regulation of CD4+ T-cells and its clinical implications
Journal name Cellular Immunology   Check publisher's open access policy
ISSN 0008-8749
Publication date 2009-01-01
Year available 2008
Sub-type Article (original research)
DOI 10.1016/j.cellimm.2008.09.001
Open Access Status DOI
Volume 254
Issue 2
Start page 85
End page 90
Total pages 6
Editor E.M. Shevach
J. Braun
Place of publication Orlando, Fla., U.S.A.
Publisher Academic Press
Language eng
Subject C1
1004 Medical Biotechnology
Abstract Interferon γ (IFNγ) plays a central role in the immune response against infection and tumur immune surveillance. Its functions include not only activation of the host immune system to control microbial infections but also repression of autoimmune responses by turning on T-regulatory cells and increasing T effector cell apoptosis. Defects in IFNγ and IFNγ receptor genes have been associated with autoimmune diseases such as rheumatoid arthritis, type 1 diabetes and multiple sclerosis. However, treatment of autoimmune diseases by supplementing with IFNγ has been satisfactory due to its broad biological effects. Instead, its target T-regulatory cells may be used for the clinical treatment of autoimmune diseases. Future study could also focus on promotion of the beneficial effects of IFNγ and blocking those unwanted IFNγ-induced activities.
Formatted abstract
Interferon γ (IFNγ) plays a central role in the immune response against infection and tumur immune surveillance. Its functions include not only activation of the host immune system to control microbial infections but also repression of autoimmune responses by turning on T-regulatory cells and increasing T effector cell apoptosis. Defects in IFNγ and IFNγ receptor genes have been associated with autoimmune diseases such as rheumatoid arthritis, type 1 diabetes and multiple sclerosis. However, treatment of autoimmune diseases by supplementing with IFNγ has been satisfactory due to its broad biological effects. Instead, its target T-regulatory cells may be used for the clinical treatment of autoimmune diseases. Future study could also focus on promotion of the beneficial effects of IFNγ and blocking those unwanted IFNγ-induced activities.
Keyword Autoimmune diseases
Rheumatoid arthritis
Q-Index Code C1
Q-Index Status Confirmed Code
Institutional Status UQ

Document type: Journal Article
Sub-type: Article (original research)
Collections: 2009 Higher Education Research Data Collection
UQ Diamantina Institute Publications
 
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Citation counts: TR Web of Science Citation Count  Cited 45 times in Thomson Reuters Web of Science Article | Citations
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Created: Thu, 11 Jun 2009, 02:52:57 EST by Siona Saplos on behalf of Office of Sponsored Research