Th2 cell-specific cytokine expression and allergen-induced airway inflammation depend on JunB

被引:126
作者
Hartenstein, B
Teurich, S
Hess, J
Schenkel, J
Schorpp-Kistner, M
Angel, P
机构
[1] Deutsch Krebsforschungszentrum, Dept Signal Transduct & Growth Control, D-69120 Heidelberg, Germany
[2] Heidelberg Univ, Inst Physiol & Pathophysiol, D-69120 Heidelberg, Germany
关键词
asthma; IL-4; IL-5; immune response; T-bet;
D O I
10.1093/emboj/cdf648
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Naive CD4+ T cells differentiate into effector T helper 1 (Th1) or Th2 cells, which are classified by their specific set of cytokines. Here we demonstrate that loss of JunB in in vitro polarized Th2 cells led to a dysregulated expression of the Th2-specific cytokines IL-4 and IL-5. These cells produce IFN-gamma and express T-bet, the key regulator of Th1 cells. In line with the essential role of Th2 cells in the pathogenesis of allergic asthma, mice with JunB-deficient CD4+ T cells exhibited an impaired allergen-induced airway inflammation. This study demonstrates novel functions of JunB in the development of Th2 effector cells, for a normal Th2 cytokine expression pattern and for a complete Th2-dependent immune response in mice.
引用
收藏
页码:6321 / 6329
页数:9
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