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. 2015 Nov 4;9(4):950–959. doi: 10.1038/mi.2015.108

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Copyright © 2016 Society for Mucosal Immunology

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IL-1R2 produced by UC-in-remission mucosa prevents IFN-γ production by C. albicans-expanded CD4⁺ T cells. (a) Representative flow cytometry dot plot from CD4⁺ cells expanded with C. albicans and autologous CD14⁺ monocytes. Intracellular staining of IFN-γ and IL-17 is shown (b) C. albicans-expanded CD4⁺ T cells were cultured with supernatants from colonic biopsies (control; n=12 or UC remission; n=12) with IL-1R2-blocking antibody (rat anti-hIL1RII-M22) or the corresponding isotype control (rat IgG2b). IFN-γ secretion was measured in culture supernatants by ELISA. Protein expression is normalized relative (%) to the isotype control condition set at 0 (line as median). Data were analyzed using a Mann–Whitney test. *P<0.05. IFN, interferon; IL, interleukin; UC, ulcerative colitis.