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Stat5 activation plays a critical role in Th2 differentiation.

Abstract：

:Upon TCR engagement, naive CD4 T cells differentiate toward the Th1 or Th2 phenotype. IL-4, acting through Stat6, plays a major role in Th2 differentiation; IL-2 has also been reported to be essential. Here, we report that retroviral (RV)-mediated expression of a constitutively active Stat5A mutant (STAT5A1*6) can fully restore IL-4 production when naive CD4 T cells are primed in the absence of IL-2. Furthermore, STAT5A1*6 expression causes Th2 differentiation in the absence of IL-4 or in Stat6- or IL-4Ralpha-deficient cells. Infection with STAT5A1*6-NGFR-RV does not enhance GATA-3 expression. STAT5A1*6-NGFR-RV and GATA-3-GFP-RV each render the Il4 gene accessible, but the sites of restriction enzyme accessibility are different. Stat5A binds to HSII and HSIII sites of the Il4 gene. Coinfection with STAT5A1*6-NGFR-RV and GATA-3-GFP-RV results in optimal Th2 priming.

journal_name

Immunity

journal_title

Immunity

authors

Zhu J,Cote-Sierra J,Guo L,Paul WE

doi

10.1016/s1074-7613(03)00292-9

keywords:

subject

Has Abstract

pub_date

2003-11-01 00:00:00

pages

739-48

issue

5

eissn

1074-7613

issn

1097-4180

pii

S1074-7613(03)00292-9

journal_volume

19

pub_type

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