TGF‐β interactions with IL‐1 family members trigger IL‐4‐independent IL‐9 production by mouse CD4+ T cells |
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| Authors: | Catherine Uyttenhove Frank Brombacher Jacques Van Snick |
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| Institution: | 1. Ludwig Institute for Cancer Research, Brussels Branch, Brussels, Belgium;2. Unité de Génétique Cellulaire, Institut de Duve, Université Catholique de Louvain, Bruxelles, Belgium;3. Division of Immunology, Institute of Infectious Disease and Molecular Medicine, Health Sciences Faculty, University of Cape Town and International Center for Genetic Engineering and Biotechnology, Cape Town, South Africa;4. Unité de Médecine Expérimentale, Institut de Duve, Université Catholique de Louvain, Bruxelles, Belgium |
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| Abstract: | TGF‐β and IL‐4 were recently shown to selectively upregulate IL‐9 production by naïve CD4+ T cells. We report here that TGF‐β interactions with IL‐1α, IL‐1β, IL‐18, and IL‐33 have equivalent IL‐9‐stimulating activities that function even in IL‐4‐deficient animals. This was observed after in vitro antigenic stimulation of immunized or unprimed mice and after polyclonal T‐cell activation. Based on intracellular IL‐9 staining, all IL‐9‐producing cells were CD4+ and 80–90% had proliferated, as indicated by reduced CFSE staining. In contrast to IL‐9, IL‐13 and IL‐17 were strongly stimulated by IL‐1 and either inhibited (IL‐13) or were unaffected (IL‐17) by addition of TGF‐β. IL‐9 and IL‐17 production also differed in their dependence on IL‐2 and regulation by IL‐1/IL‐23. As IL‐9 levels were much lower in Th2 and Th17 cultures, our results identify TGF‐β/IL‐1 and TGF‐β/IL‐4 as the main control points of IL‐9 synthesis. |
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| Keywords: | IL‐1 family IL‐9 regulation TGF‐β |
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