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,**,¶
Departments of
* Molecular Immunology,
Medical Immunology, and
General Surgery, Graduate School of Medicine, Chiba University, Chiba, Japan;
PRESTO, Tokyo, Japan;
¶ CREST Japan Science and Technology Corp., Tokyo, Japan;
|| Laboratory for Immune Regulation, RIKEN Research Center for Allergy and Immunology, Tokyo, Japan;
# Department of Tropical Medicine, Jikei University School of Medicine, Tokyo, Japan; and
** Section of Allergy, Immunology and Rheumatology, Department of Internal Medicine, Medical College, National Cheng Kung University, Tainan, Taiwan
The central role for Th2 cells in the development of Ag-induced airway hyperresponsiveness and eosinophilic inflammation is well documented. We have reported a crucial role for TCR-induced activation of the Ras/extracellular signal-regulated kinase mitogen-activated protein kinase cascade in Th2 cell differentiation. Here, we show that the development of both OVA-induced airway hyperresponsiveness and eosinophilic airway inflammation in a mouse asthma model are attenuated in transgenic mice by the overexpression of enzymatically inactive Ras molecules in T cells. In addition, reduced levels of IL-5 production and eosinophilic inflammation induced by nematode infection (Nippostrongylus brasiliensis or Heligmosomoides polygyrus) were detected. Thus, the level of Ras activation in T cells appears to determine Th2-dependent eosinophilic inflammation and Ag-induced airway hyperresponsiveness.
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