Kurzfassung

Asthma is a disease that is notable for augmented Th2 and impaired Th1 cytokine responses. A possible explanation for the altered Th1 responses in asthma may relate to altered T-bet, IL-12 levels and IL-12 signal transduction. Release of IL-12 (p40/p35) from antigen-presenting cells directs the differentiation of T cells into Th1 cells with up-regulation of IFN-gamma transcription and secretion.
NFATc2 studies in asthma: We demonstrate that mice lacking nuclear factor of activated T cells-2...Asthma is a disease that is notable for augmented Th2 and impaired Th1 cytokine responses. A possible explanation for the altered Th1 responses in asthma may relate to altered T-bet, IL-12 levels and IL-12 signal transduction. Release of IL-12 (p40/p35) from antigen-presenting cells directs the differentiation of T cells into Th1 cells with up-regulation of IFN-gamma transcription and secretion.
NFATc2 studies in asthma: We demonstrate that mice lacking nuclear factor of activated T cells-2 (NFATc2) developed increased airway hyperresponsiveness (AHR) and had increased serum IgE levels in the absence of exogenous allergen challenge. This AHR was associated both with activated, hyperproliferative lung CD4+ Th2 cells but also with CD8+ T cells defective in interferon-gamma (IFN-gamma production).
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