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• W2101735643 abstract "Gaudenzio et al1Gaudenzio N. Laurent C. Valitutti S. Espinosa E. Human mast cells drive memory CD4+ T cells toward an inflammatory IL-22+ phenotype.J Allergy Clin Immunol. 2013; 131: 1400-1407.e11Abstract Full Text Full Text PDF PubMed Scopus (50) Google Scholar reported that human mast cells drive memory CD4+ T cells toward IL-22 producers. They found that mast cells form synaptic-like contacts with CD4+ T cells and promote IL-22–producing CD4+ T cells through a TNF-α/IL-6–dependent mechanism. Thus these results point toward a role for mast cells in driving TH responses in inflammatory conditions.Tissue-resident mast cells share several common features with basophils.2Voehringer D. Protective and pathological roles of mast cells and basophils.Nat Rev Immunol. 2013; 13: 362-375Crossref PubMed Scopus (269) Google Scholar, 3Karasuyama H. Mukai K. Obata K. Tsujimura Y. Wada T. Nonredundant roles of basophils in immunity.Annu Rev Immunol. 2011; 29: 45-69Crossref PubMed Scopus (183) Google Scholar Both types of cells release various cytokines on activation, including IL-4, IL-6, and IL-13; express common receptors, such as FcεRI, CD200R3, C3aR, C5aR, IL-3 receptor, IL-18 receptor, and IL-33 receptor; and release several inflammatory mediators, such as histamine and leukotrienes. In addition, basophils are also known to recruit to the inflamed tissues. In view of these common features, similar activation mechanisms, and cytokine profiles, we explored whether human basophils, similar to mast cells, possess the capacity to promote IL-22 responses from CD4+ T cells.First, we examined the direct effect of basophils on IL-22 responses from CD4+CD45RO+CD25− memory T cells. Basophils were activated either by IL-3 alone or through IL-3 and FcεRI cross-linking (see the Methods section in this article's Online Repository at www.jacionline.org). We found that neither IL-3–primed nor FcεRI-activated basophils alone could promote IL-22 from memory CD4+ T cells (Fig 1). These results imply that unlike mast cells, basophils are poor inducers of IL-22 responses from CD4+ T cells.Activation and expansion of CD4+ T cells implicate coordination of 4 different signals, including activation of professional antigen-presenting cells (APCs) through pattern-recognition receptors (signal zero), interactions of antigen-loaded HLA-DR with T-cell receptor–CD3 complexes (signal 1) and costimulatory molecules (signal 2), and signaling events mediated by T cell–polarizing cytokines (signal 3). Several reports, including ours, have recently demonstrated that circulating human basophils lack the features of APCs to mediate T-cell responses. This inability of basophils to promote T-cell responses was mainly due to the absence of HLA-DR and the costimulatory molecules CD80 and CD86. Thus the lack of T-cell receptor– and costimulatory molecule–mediated signals might explain the inability of human basophils to mediate IL-22 responses.4Kitzmuller C. Nagl B. Deifl S. Walterskirchen C. Jahn-Schmid B. Zlabinger G.J. et al.Human blood basophils do not act as antigen-presenting cells for the major birch pollen allergen Bet v 1.Allergy. 2012; 67: 593-600Crossref PubMed Scopus (52) Google Scholar, 5Sharma M. Hegde P. Aimanianda V. Beau R. Mohan M.S. Senechal H. et al.Circulating human basophils lack the features of professional antigen presenting cells.Sci Rep. 2013; 3: 1188PubMed Google ScholarHowever, the above results did not provide clues on the indirect effect of basophils in promoting APC-mediated IL-22 responses. Therefore by using Toll-like receptor (TLR)–activated monocytes, we determined whether circulating human basophils are capable of enhancing IL-22 from CD4+ T cells. Monocytes were pulsed with the TLR2 agonist peptidoglycan and subsequently cocultured with memory CD4+ T cells either in the presence or absence of activated basophils. We found that TLR-activated monocytes promoted IL-22 from memory CD4+ T cells. However, IL-3–treated basophils did not further amplify monocyte-mediated IL-22 responses (Fig 1). Similar results were also obtained in the presence of FcεRI-activated basophils. These results suggest that circulating human basophils lack the ability to augment APC-mediated IL-22 responses.In summary, our data indicate that although basophils share several common properties with mast cells, unlike these cells, basophils do not possess the capacity to drive memory CD4+ T cells toward IL-22 producers, either directly or through APCs. Gaudenzio et al1Gaudenzio N. Laurent C. Valitutti S. Espinosa E. Human mast cells drive memory CD4+ T cells toward an inflammatory IL-22+ phenotype.J Allergy Clin Immunol. 2013; 131: 1400-1407.e11Abstract Full Text Full Text PDF PubMed Scopus (50) Google Scholar reported that human mast cells drive memory CD4+ T cells toward IL-22 producers. They found that mast cells form synaptic-like contacts with CD4+ T cells and promote IL-22–producing CD4+ T cells through a TNF-α/IL-6–dependent mechanism. Thus these results point toward a role for mast cells in driving TH responses in inflammatory conditions. Tissue-resident mast cells share several common features with basophils.2Voehringer D. Protective and pathological roles of mast cells and basophils.Nat Rev Immunol. 2013; 13: 362-375Crossref PubMed Scopus (269) Google Scholar, 3Karasuyama H. Mukai K. Obata K. Tsujimura Y. Wada T. Nonredundant roles of basophils in immunity.Annu Rev Immunol. 2011; 29: 45-69Crossref PubMed Scopus (183) Google Scholar Both types of cells release various cytokines on activation, including IL-4, IL-6, and IL-13; express common receptors, such as FcεRI, CD200R3, C3aR, C5aR, IL-3 receptor, IL-18 receptor, and IL-33 receptor; and release several inflammatory mediators, such as histamine and leukotrienes. In addition, basophils are also known to recruit to the inflamed tissues. In view of these common features, similar activation mechanisms, and cytokine profiles, we explored whether human basophils, similar to mast cells, possess the capacity to promote IL-22 responses from CD4+ T cells. First, we examined the direct effect of basophils on IL-22 responses from CD4+CD45RO+CD25− memory T cells. Basophils were activated either by IL-3 alone or through IL-3 and FcεRI cross-linking (see the Methods section in this article's Online Repository at www.jacionline.org). We found that neither IL-3–primed nor FcεRI-activated basophils alone could promote IL-22 from memory CD4+ T cells (Fig 1). These results imply that unlike mast cells, basophils are poor inducers of IL-22 responses from CD4+ T cells. Activation and expansion of CD4+ T cells implicate coordination of 4 different signals, including activation of professional antigen-presenting cells (APCs) through pattern-recognition receptors (signal zero), interactions of antigen-loaded HLA-DR with T-cell receptor–CD3 complexes (signal 1) and costimulatory molecules (signal 2), and signaling events mediated by T cell–polarizing cytokines (signal 3). Several reports, including ours, have recently demonstrated that circulating human basophils lack the features of APCs to mediate T-cell responses. This inability of basophils to promote T-cell responses was mainly due to the absence of HLA-DR and the costimulatory molecules CD80 and CD86. Thus the lack of T-cell receptor– and costimulatory molecule–mediated signals might explain the inability of human basophils to mediate IL-22 responses.4Kitzmuller C. Nagl B. Deifl S. Walterskirchen C. Jahn-Schmid B. Zlabinger G.J. et al.Human blood basophils do not act as antigen-presenting cells for the major birch pollen allergen Bet v 1.Allergy. 2012; 67: 593-600Crossref PubMed Scopus (52) Google Scholar, 5Sharma M. Hegde P. Aimanianda V. Beau R. Mohan M.S. Senechal H. et al.Circulating human basophils lack the features of professional antigen presenting cells.Sci Rep. 2013; 3: 1188PubMed Google Scholar However, the above results did not provide clues on the indirect effect of basophils in promoting APC-mediated IL-22 responses. Therefore by using Toll-like receptor (TLR)–activated monocytes, we determined whether circulating human basophils are capable of enhancing IL-22 from CD4+ T cells. Monocytes were pulsed with the TLR2 agonist peptidoglycan and subsequently cocultured with memory CD4+ T cells either in the presence or absence of activated basophils. We found that TLR-activated monocytes promoted IL-22 from memory CD4+ T cells. However, IL-3–treated basophils did not further amplify monocyte-mediated IL-22 responses (Fig 1). Similar results were also obtained in the presence of FcεRI-activated basophils. These results suggest that circulating human basophils lack the ability to augment APC-mediated IL-22 responses. In summary, our data indicate that although basophils share several common properties with mast cells, unlike these cells, basophils do not possess the capacity to drive memory CD4+ T cells toward IL-22 producers, either directly or through APCs. MethodsIsolation of circulating human basophils, monocytes, and memory T cellsBuffy bags from healthy donors were obtained from Centre Necker-Cabanel, Etablissement Français du Sang, Paris, France. Ethics committee permission was obtained for the use of these buffy bags (no. 12/EFS/079). Basophil-rich fractions of PBMCs were obtained by using Percoll density gradient centrifugation. Basophils from these basophil-rich PBMCs were isolated by using the Basophil Isolation Kit II (Miltenyi Biotec, Paris, France). Monocytes were isolated from PBMCs by using CD14 magnetic microbeads (Miltenyi Biotec). For isolation of memory T cells, untouched total CD4+ T cells were purified by means of negative selection with the CD4+ T Cell Isolation Kit II (Miltenyi Biotec). Furthermore, untagged memory (CD45RO+) T cells were subsequently isolated from total CD4+ T cells by positively selecting naive (CD45RA+) T cells with CD45RA microbeads (Miltenyi Biotec). Finally, CD4+CD45RO+CD25− memory T cells were obtained by depleting CD25+ cells with CD25 microbeads (Miltenyi Biotec). The purity of various cellular populations was greater than 95%.Coculture of basophils and monocytes with CD4+CD45RO+CD25− memory T cellsCD4+CD45RO+CD25− memory T cells were cultured in U-bottom, 96-well plates (0.1 × 106 cells/200 μL per well) in X-vivo-10% AB serum and IL-2 (100 IU/mL) either alone or with IL-3 (100 ng/106 cells)–primed basophils, with IL-3 and anti-IgE (10 ng/0.1 million cells)–treated basophils, with monocytes stimulated with peptidoglycan (5 μg/0.5 million cells), with peptidoglycan-stimulated monocytes and IL-3–primed basophils, or with peptidoglycan-stimulated monocytes along with IL-3 and anti-IgE–treated basophils. The ratio of T cells and monocytes or basophils was maintained at 5:1. After 4 to 5 days of culture, cell-free culture supernatants were collected for analysis of IL-22.IL-22 analysisLevels of IL-22 (ELISA Ready-SET-Go; eBioscience, San Diego, Calif) in cell-free culture supernatants were quantified by means of ELISA. The detection limit was 8 pg/mL.Statistical analysisThe significance of differences was assessed by using 1-way ANOVA, and comparison between sets of results was assessed by using the Tukey post-test. P values of less than .05 were considered statistically correlated. Prism 5 software (GraphPad Software, La Jolla, Calif) was used for statistical analyses. Isolation of circulating human basophils, monocytes, and memory T cellsBuffy bags from healthy donors were obtained from Centre Necker-Cabanel, Etablissement Français du Sang, Paris, France. Ethics committee permission was obtained for the use of these buffy bags (no. 12/EFS/079). Basophil-rich fractions of PBMCs were obtained by using Percoll density gradient centrifugation. Basophils from these basophil-rich PBMCs were isolated by using the Basophil Isolation Kit II (Miltenyi Biotec, Paris, France). Monocytes were isolated from PBMCs by using CD14 magnetic microbeads (Miltenyi Biotec). For isolation of memory T cells, untouched total CD4+ T cells were purified by means of negative selection with the CD4+ T Cell Isolation Kit II (Miltenyi Biotec). Furthermore, untagged memory (CD45RO+) T cells were subsequently isolated from total CD4+ T cells by positively selecting naive (CD45RA+) T cells with CD45RA microbeads (Miltenyi Biotec). Finally, CD4+CD45RO+CD25− memory T cells were obtained by depleting CD25+ cells with CD25 microbeads (Miltenyi Biotec). The purity of various cellular populations was greater than 95%. Buffy bags from healthy donors were obtained from Centre Necker-Cabanel, Etablissement Français du Sang, Paris, France. Ethics committee permission was obtained for the use of these buffy bags (no. 12/EFS/079). Basophil-rich fractions of PBMCs were obtained by using Percoll density gradient centrifugation. Basophils from these basophil-rich PBMCs were isolated by using the Basophil Isolation Kit II (Miltenyi Biotec, Paris, France). Monocytes were isolated from PBMCs by using CD14 magnetic microbeads (Miltenyi Biotec). For isolation of memory T cells, untouched total CD4+ T cells were purified by means of negative selection with the CD4+ T Cell Isolation Kit II (Miltenyi Biotec). Furthermore, untagged memory (CD45RO+) T cells were subsequently isolated from total CD4+ T cells by positively selecting naive (CD45RA+) T cells with CD45RA microbeads (Miltenyi Biotec). Finally, CD4+CD45RO+CD25− memory T cells were obtained by depleting CD25+ cells with CD25 microbeads (Miltenyi Biotec). The purity of various cellular populations was greater than 95%. Coculture of basophils and monocytes with CD4+CD45RO+CD25− memory T cellsCD4+CD45RO+CD25− memory T cells were cultured in U-bottom, 96-well plates (0.1 × 106 cells/200 μL per well) in X-vivo-10% AB serum and IL-2 (100 IU/mL) either alone or with IL-3 (100 ng/106 cells)–primed basophils, with IL-3 and anti-IgE (10 ng/0.1 million cells)–treated basophils, with monocytes stimulated with peptidoglycan (5 μg/0.5 million cells), with peptidoglycan-stimulated monocytes and IL-3–primed basophils, or with peptidoglycan-stimulated monocytes along with IL-3 and anti-IgE–treated basophils. The ratio of T cells and monocytes or basophils was maintained at 5:1. After 4 to 5 days of culture, cell-free culture supernatants were collected for analysis of IL-22. CD4+CD45RO+CD25− memory T cells were cultured in U-bottom, 96-well plates (0.1 × 106 cells/200 μL per well) in X-vivo-10% AB serum and IL-2 (100 IU/mL) either alone or with IL-3 (100 ng/106 cells)–primed basophils, with IL-3 and anti-IgE (10 ng/0.1 million cells)–treated basophils, with monocytes stimulated with peptidoglycan (5 μg/0.5 million cells), with peptidoglycan-stimulated monocytes and IL-3–primed basophils, or with peptidoglycan-stimulated monocytes along with IL-3 and anti-IgE–treated basophils. The ratio of T cells and monocytes or basophils was maintained at 5:1. After 4 to 5 days of culture, cell-free culture supernatants were collected for analysis of IL-22. IL-22 analysisLevels of IL-22 (ELISA Ready-SET-Go; eBioscience, San Diego, Calif) in cell-free culture supernatants were quantified by means of ELISA. The detection limit was 8 pg/mL. Levels of IL-22 (ELISA Ready-SET-Go; eBioscience, San Diego, Calif) in cell-free culture supernatants were quantified by means of ELISA. The detection limit was 8 pg/mL. Statistical analysisThe significance of differences was assessed by using 1-way ANOVA, and comparison between sets of results was assessed by using the Tukey post-test. P values of less than .05 were considered statistically correlated. Prism 5 software (GraphPad Software, La Jolla, Calif) was used for statistical analyses. The significance of differences was assessed by using 1-way ANOVA, and comparison between sets of results was assessed by using the Tukey post-test. P values of less than .05 were considered statistically correlated. Prism 5 software (GraphPad Software, La Jolla, Calif) was used for statistical analyses. Human mast cells drive memory CD4+ T cells toward an inflammatory IL-22+ phenotypeJournal of Allergy and Clinical ImmunologyVol. 131Issue 5PreviewMast cells are key components of the skin microenvironment in psoriasis, yet their functional role in this T-cell–mediated inflammatory disorder remains to be elucidated. Full-Text PDF ReplyJournal of Allergy and Clinical ImmunologyVol. 132Issue 6PreviewWe thank Sharma et al1 for their interest in our recently published article.2 In our study we demonstrate that primary human mast cells can express MHC class II and costimulatory molecules upon treatment with IFN-γ and can form functional immunologic synapses with previously activated T cells. We also show that cognate interaction between mast cells and freshly isolated memory CD4+ T cells leads to the generation of TH22 and IL-22/IFN-γ–producing TH cells.2 In addition, we previously demonstrated that IFN-γ–primed mouse mast cells express MHC class II and costimulatory molecules and form immunologic synapses with antigen-experienced CD4+ T cells. Full-Text PDF" @default.
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