Interferon γ stabilizes the T helper cell type 1 phenotype

被引：68

作者：

Zhang, YK

Apilado, R

Coleman, J

Ben-Sasson, S

Tsang, S

Hu-Li, J

Paul, WE

Huang, H

机构：

[1] Loyola Univ, Stritch Sch Med, Dept Cell Biol Neurobiol & Anat, Maywood, IL 60153 USA

[2] NIAID, Immunol Lab, NIH, Bethesda, MD 20892 USA

[3] Hebrew Univ Jerusalem, Sch Med, Lautenberg Ctr Gen & Tumor Immunol, IL-91120 Jerusalem, Israel

来源：

JOURNAL OF EXPERIMENTAL MEDICINE | 2001年 / 194卷 / 02期

关键词：

IL-4; IL-12; differentiation; commitment; cell cloning;

D O I：

10.1084/jem.194.2.165

中图分类号：

R392 [医学免疫学]; Q939.91 [免疫学];

学科分类号：

100102 ;

摘要：

T helper cell (Th)1-primed CD4 T cells from wild-type donors make little interleukin (IL)-4 when restimulated under Th2 conditions. However, such restimulation of Th1-primed cells from interferon (IFN)-gamma (-/-) or IFN-gamma receptor (IFN-gammaR)(-/-) mice resulted in substantial production of IL-4 and other Th2 cytokines. Adding IFN-gamma to the priming culture markedly diminished the capacity of Th1-primed IFN-gamma (-/-) cells to express IL-4. Even IFN-gamma -producing cells from IFN-gammaR(-/-) mice could acquire IL-4-producing capacity. Thus, IFN-gamma is not required for the development of IFN-gamma -producing capacity, but it plays a critical role in suppressing the IL-4-producing potential of Th1 cells.

引用

收藏

页码：165 / 172

页数：8

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