GATA-3 deficiency abrogates the development and maintenance of T helper type 2 cells

被引：285

作者：

Pai, SY

Truitt, ML

Ho, IC ^{[1
]}

机构：

[1] Harvard Univ, Sch Med, Boston, MA 02115 USA

[2] Dana Farber Canc Inst, Dept Pediat Hematol Oncol, Boston, MA 02115 USA

[3] Childrens Hosp, Boston, MA 02115 USA

[4] Harvard Univ, Sch Publ Hlth, Dept Immunol & Infect Dis, Boston, MA 02115 USA

[5] Brigham & Womens Hosp, Dept Rheumatol Immunol & Allergy, Boston, MA 02115 USA

来源：

PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA | 2004年 / 101卷 / 07期

关键词：

D O I：

10.1073/pnas.0308697100

中图分类号：

O [数理科学和化学]; P [天文学、地球科学]; Q [生物科学]; N [自然科学总论];

学科分类号：

07 ; 0710 ; 09 ;

摘要：

T helper type 2 (Th2) cells secrete IL-4, IL-5, IL-10, and IL-13 and mediate allergic and asthmatic disease. GATA-3 is a Th2-specific transcription factor that appears in overexpression studies and transgenic systems to function as a Th2 lineage determinant. Because GATA-3 is also crucial for development of the T lineage and throughout thymic development, direct demonstration that GATA-3 is required for Th2 development by targeted deletion has been lacking. Using a conditional knockout approach, we found that GATA-3 is required for optimal Th2 cytokine production in vitro and in vivo. Our data also show that GATA-3 expression must be sustained to maintain the Th2 phenotype.

引用

页码：1993 / 1998

页数：6

共 38 条

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