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The Chemokine Receptor CXCR6 Controls the Functional Topography of Interleukin-22 Producing Intestinal Innate Lymphoid Cells

Abstract : SUMMARY Interleukin-22 (IL-22) plays a critical role in mucosal defense, although the molecular mechanisms that ensure IL-22 tissue distribution remain poorly under-stood. We show that the CXCL16-CXCR6 chemo-kine-chemokine receptor axis regulated group 3 innate lymphoid cell (ILC3) diversity and function. CXCL16 was constitutively expressed by CX3CR1 + intestinal dendritic cells (DCs) and coexpressed with IL-23 after Citrobacter rodentium infection. In-testinal ILC3s expressed CXCR6 and its ablation generated a selective loss of the NKp46 + ILC3 subset, a depletion of intestinal IL-22, and the inability to control C. rodentium infection. CD4 + ILC3s were unaffected by CXCR6 deficiency and remained clustered within lymphoid follicles. In contrast, the lamina propria of Cxcr6 À/À mice was devoid of ILC3s. The loss of ILC3-dependent IL-22 epithelial stimulation reduced antimicrobial peptide expression that explained the sensitivity of Cxcr6 À/À mice to C. rodentium. Our results delineate a critical CXCL16-CXCR6 crosstalk that coordinates the intes-tinal topography of IL-22 secretion required for mucosal defense.
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Submitted on : Wednesday, December 3, 2014 - 2:59:37 PM
Last modification on : Thursday, April 7, 2022 - 10:10:21 AM
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Naoko Satoh-Takayama, Nicolas Serafini, Thomas Verrier, Abdessalem Rekiki, Jean-Christophe Renauld, et al.. The Chemokine Receptor CXCR6 Controls the Functional Topography of Interleukin-22 Producing Intestinal Innate Lymphoid Cells. Immunity, Elsevier, 2014, 41, pp.776-788. ⟨10.1016/j.immuni.2014.10.007⟩. ⟨pasteur-01090414⟩

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