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Article

  • The EMBO Journal (2002) 21, 6321 - 6329
  • doi:10.1093/emboj/cdf648

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

Bettina Hartenstein1, Sibylle Teurich1, Jochen Hess1, Johannes Schenkel2, Marina Schorpp-Kistner1 and Peter Angel1

  1. Deutsches Krebsforschungszentrum Heidelberg, Department of Signal Transduction and Growth Control, Im Neuenheimer Feld 280, D-69120 Heidelberg Germany
  2. Institute of Physiology and Pathophysiology, Heidelberg University, Im Neuenheimer Feld 326, D-69120 Heidelberg, Germany

Correspondence to:

Peter Angel, E-mail: p.angel@dkfz-heidelberg.de

Received 9 August 2002; Accepted 16 October 2002; Revised 15 October 2002

Naïve 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.

  • Keywords:

    • asthma,
    • IL-4,
    • IL-5,
    • immune response,
    • T-bet