Innate lymphoid cells (ILC) are important sources of effector cytokines during homeostasis and diverse inflammatory conditions. A specialized group of ILC, the Group 3 ILC (ILC3), produces IL-22 and IL-17A, and contributes to maintenance of the gut epithelial barrier and the host response to extracellular microbes. ILC3s express Tnfsf11, a type II receptor required for osteoclastogenesis. The functions of Tnfsf11 in ILC3s are not fully understood. Here we show that Tnfsf11-deficient ILC3s are hyperproliferative and express altered cell surface markers at steady state. Additionally, Tnfsf11-deficient ILC3s produce increased amounts of effector cytokines in response to the activating cytokine IL-23. Although mature osteoclast-, lymph node-, and M cell-development are dysfunctional in Tnfsf11−/− mice, Tnfsf11 expression is not required in ILC3s for these developmental pathways. Thus, Tnfsf11 regulates ILC3 homeostasis in the gut.
Citation Format: Jennifer K. Bando, Christina Song, Susan Gilfillan, Marco Colonna. Roles for Tnfsf11 expression by group 3 innate lymphoid cells [abstract]. In: Proceedings of the Second CRI-CIMT-EATI-AACR International Cancer Immunotherapy Conference: Translating Science into Survival; 2016 Sept 25-28; New York, NY. Philadelphia (PA): AACR; Cancer Immunol Res 2016;4(11 Suppl):Abstract nr B124.
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