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T Cells from Human Allergen-Induced Late Asthmatic Responses Express IL-12 Receptor ß2 Subunit mRNA and Respond to IL-12 In Vitro¹

Eva Maria Varga^*, Petra Wachholz^*, Kayhan T. Nouri-Aria^*, Adrienne Verhoef^*, Christopher J. Corrigan, Stephen J. Till^* and Stephen R. Durham^2,*

^* Upper Respiratory Medicine, Imperial College School of Medicine at National Heart and Lung Institute, London, United Kingdom; and Department of Allergy and Respiratory Medicine, Guy’s Hospital, London, United Kingdom

IL-12 suppresses proallergic Th2-type cytokine production and induces Th1-type cytokine production by peripheral blood T cells from subjects with allergic disease. The objective of the present study was to examine the relevance of these findings to target organ T cell responses in human asthma. Bronchoalveolar lavage (BAL) and PBMC were collected from atopic asthmatics 24 h after fiberoptic allergen challenge of a segmental bronchus. BAL T cells and PBMC were cultured with allergen in the presence of recombinant IL-12 or IFN-, and cytokines were measured in culture supernatants after 6 days. IL-5 production by BAL T cells and PBMC was inhibited by IL-12 and, to a lesser extent, by IFN-. IL-12 also induced IFN- production by BAL T cells and PBMC. The effects of IL-12 nor IFN- on IL-5 production could not be reversed by neutralizing anti-IFN- or anti-IL-12 mAbs, respectively. Thus, the effect of neither IL-12 nor IFN- appeared to be mediated through induction of the other cytokine. In situ hybridization revealed that approximately one-third of BAL T cells expressed mRNA transcripts encoding the IL-12R ß2 subunit following allergen challenge. Thus, human T cells obtained from BAL during asthmatic late responses, like T cells in the peripheral circulation, remain susceptible to immunomodulation by IL-12. These findings raise the possibility that IL-12 may hold therapeutic potential in allergic diseases such as asthma.

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