共 38 条
GATA-3 deficiency abrogates the development and maintenance of T helper type 2 cells
被引:285
作者:

Pai, SY
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机构: Harvard Univ, Sch Med, Boston, MA 02115 USA

Truitt, ML
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机构: Harvard Univ, Sch Med, Boston, MA 02115 USA

Ho, IC
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机构:
Harvard Univ, Sch Med, Boston, MA 02115 USA Harvard Univ, Sch Med, Boston, MA 02115 USA
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:
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.
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页码:1993 / 1998
页数:6
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