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Background  Inducible Costimulator (ICOS) is an important regulator of Th2 lymphocyte function and a potential immunotherapeutic target for allergy and asthma. A SNP in the  ICOS  5′ promoter in humans is associated with increased atopy and serum IgE in a founder population and increased ICOS surface expression and Th2 cytokine production from peripheral blood mononuclear cells. However, it is unknown if increased ICOS expression contributes to disease progression or is a result of disease pathology.    Methodology/Principal Findings  We developed a mouse model in which ICOS surface expression levels are genetically predetermined to test our hypothesis that genetic regulation of ICOS expression controls the severity of Th2 responses  in vivo . Using ICOS +/+  and ICOS +/−  mice in a Th2 model of airway inflammation, we found that T cells from the ICOS +/−  mice had reduced ICOS expression and decreased Th2-mediated inflammation  in vivo . Although the activation status of the T cells did not differ, T cells isolated from the lungs and draining lymph nodes of ICOS +/−  mice at the peak of inflammation produced less Th2 cytokines upon stimulation  ex vivo . Using 4get mice, which express GFP upon IL-4 transcription, we determined that the decreased Th2 cytokines in ICOS +/−  is due to reduced percentage of Th2 cells and not a defect in their ability to produce IL-4.    Conclusion  These data suggest that in both mice and humans, the level of ICOS surface expression regulates the magnitude of the  in vivo  Th2 response, perhaps by influencing Th2 differentiation.

Inducible Costimulator Expression Regulates the Magnitude of Th2-Mediated Airway Inflammation by Regulating the Number of Th2 Cells