Homeostatic IL-13 in healthy skin directs dendritic cell differentiation to promote T\textlessinf\textgreaterH\textless/inf\textgreater2 and inhibit T\textlessinf\textgreaterH\textless/inf\textgreater17 cell polarization. Mayer, J., Hilligan, K., Chandler, J., Eccles, D., Old, S., Domingues, R., Yang, J., Webb, G., Munoz-Erazo, L., Hyde, E., Lamiable, O., & Ronchese, F. Nature Immunology, 22(12):1538–1550, 2021. doi abstract bibtex The signals driving the adaptation of type 2 dendritic cells (DC2s) to diverse peripheral environments remain mostly undefined. We show that differentiation of CD11blo migratory DC2s—a DC2 population unique to the dermis—required IL-13 signaling dependent on the transcription factors STAT6 and KLF4, whereas DC2s in lung and small intestine were STAT6-independent. Similarly, human DC2s in skin expressed an IL-4 and IL-13 gene signature that was not found in blood, spleen and lung DCs. In mice, IL-13 was secreted homeostatically by dermal innate lymphoid cells and was independent of microbiota, TSLP or IL-33. In the absence of IL-13 signaling, dermal DC2s were stable in number but remained CD11bhi and showed defective activation in response to allergens, with diminished ability to support the development of IL-4+GATA3+ helper T cells (TH), whereas antifungal IL-17+ROR$γ$t+ TH cells were increased. Therefore, homeostatic IL-13 fosters a noninflammatory skin environment that supports allergic sensitization.
@article{Mayer2021a,
abstract = {The signals driving the adaptation of type 2 dendritic cells (DC2s) to diverse peripheral environments remain mostly undefined. We show that differentiation of CD11blo migratory DC2s—a DC2 population unique to the dermis—required IL-13 signaling dependent on the transcription factors STAT6 and KLF4, whereas DC2s in lung and small intestine were STAT6-independent. Similarly, human DC2s in skin expressed an IL-4 and IL-13 gene signature that was not found in blood, spleen and lung DCs. In mice, IL-13 was secreted homeostatically by dermal innate lymphoid cells and was independent of microbiota, TSLP or IL-33. In the absence of IL-13 signaling, dermal DC2s were stable in number but remained CD11bhi and showed defective activation in response to allergens, with diminished ability to support the development of IL-4+GATA3+ helper T cells (TH), whereas antifungal IL-17+ROR$\gamma$t+ TH cells were increased. Therefore, homeostatic IL-13 fosters a noninflammatory skin environment that supports allergic sensitization.},
author = {Mayer, J.U. and Hilligan, K.L. and Chandler, J.S. and Eccles, D.A. and Old, S.I. and Domingues, R.G. and Yang, J. and Webb, G.R. and Munoz-Erazo, L. and Hyde, E.J. and Lamiable, O. and Ronchese, F.},
doi = {10.1038/s41590-021-01067-0},
journal = {Nature Immunology},
number = {12},
pages = {1538--1550},
title = {{Homeostatic IL-13 in healthy skin directs dendritic cell differentiation to promote T{\textless}inf{\textgreater}H{\textless}/inf{\textgreater}2 and inhibit T{\textless}inf{\textgreater}H{\textless}/inf{\textgreater}17 cell polarization}},
volume = {22},
year = {2021}
}
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Similarly, human DC2s in skin expressed an IL-4 and IL-13 gene signature that was not found in blood, spleen and lung DCs. In mice, IL-13 was secreted homeostatically by dermal innate lymphoid cells and was independent of microbiota, TSLP or IL-33. In the absence of IL-13 signaling, dermal DC2s were stable in number but remained CD11bhi and showed defective activation in response to allergens, with diminished ability to support the development of IL-4+GATA3+ helper T cells (TH), whereas antifungal IL-17+ROR$γ$t+ TH cells were increased. Therefore, homeostatic IL-13 fosters a noninflammatory skin environment that supports allergic sensitization.","author":[{"propositions":[],"lastnames":["Mayer"],"firstnames":["J.U."],"suffixes":[]},{"propositions":[],"lastnames":["Hilligan"],"firstnames":["K.L."],"suffixes":[]},{"propositions":[],"lastnames":["Chandler"],"firstnames":["J.S."],"suffixes":[]},{"propositions":[],"lastnames":["Eccles"],"firstnames":["D.A."],"suffixes":[]},{"propositions":[],"lastnames":["Old"],"firstnames":["S.I."],"suffixes":[]},{"propositions":[],"lastnames":["Domingues"],"firstnames":["R.G."],"suffixes":[]},{"propositions":[],"lastnames":["Yang"],"firstnames":["J."],"suffixes":[]},{"propositions":[],"lastnames":["Webb"],"firstnames":["G.R."],"suffixes":[]},{"propositions":[],"lastnames":["Munoz-Erazo"],"firstnames":["L."],"suffixes":[]},{"propositions":[],"lastnames":["Hyde"],"firstnames":["E.J."],"suffixes":[]},{"propositions":[],"lastnames":["Lamiable"],"firstnames":["O."],"suffixes":[]},{"propositions":[],"lastnames":["Ronchese"],"firstnames":["F."],"suffixes":[]}],"doi":"10.1038/s41590-021-01067-0","journal":"Nature Immunology","number":"12","pages":"1538–1550","title":"Homeostatic IL-13 in healthy skin directs dendritic cell differentiation to promote T\\textlessinf\\textgreaterH\\textless/inf\\textgreater2 and inhibit T\\textlessinf\\textgreaterH\\textless/inf\\textgreater17 cell polarization","volume":"22","year":"2021","bibtex":"@article{Mayer2021a,\nabstract = {The signals driving the adaptation of type 2 dendritic cells (DC2s) to diverse peripheral environments remain mostly undefined. We show that differentiation of CD11blo migratory DC2s—a DC2 population unique to the dermis—required IL-13 signaling dependent on the transcription factors STAT6 and KLF4, whereas DC2s in lung and small intestine were STAT6-independent. Similarly, human DC2s in skin expressed an IL-4 and IL-13 gene signature that was not found in blood, spleen and lung DCs. In mice, IL-13 was secreted homeostatically by dermal innate lymphoid cells and was independent of microbiota, TSLP or IL-33. In the absence of IL-13 signaling, dermal DC2s were stable in number but remained CD11bhi and showed defective activation in response to allergens, with diminished ability to support the development of IL-4+GATA3+ helper T cells (TH), whereas antifungal IL-17+ROR$\\gamma$t+ TH cells were increased. 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