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Host resistance to endotoxic shock requires the neuroendocrine regulation of group 1 innate lymphoid cells

Abstract : Upon infection, the immune system produces inflammatory mediators important for pathogen clearance. However, inflammation can also have deleterious effect on the host and is tightly regulated. Immune system-derived cytokines stimulate the hypothalamic-pituitary-adrenal (HPA) axis, triggering endogenous glucocorticoid production. Through interaction with ubiquitously expressed glucocorticoid receptors (GRs), this steroid hormone has pleiotropic effects on many cell types. Using a genetic mouse model in which the gene encoding the GR is selectively deleted in NKp46(+) innate lymphoid cells (ILCs), we demonstrated a major role for the HPA pathway in host resistance to endotoxin-induced septic shock. GR expression in group 1 ILCs is required to limit their IFN-gamma production, thereby allowing the development of IL-10-dependent tolerance to endotoxin. These findings suggest that neuroendocrine axes are crucial for tolerization of the innate immune system to microbial endotoxin exposure through direct corticosterone-mediated effects on NKp46-expressing innate cells, revealing a novel strategy of host protection from immunopathology.
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Submitted on : Friday, April 13, 2018 - 11:08:39 AM
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Linda Quatrini, Elisabeth Wieduwild, Sophie Guia, Claire Bernat, Nicolas Glaichenhaus, et al.. Host resistance to endotoxic shock requires the neuroendocrine regulation of group 1 innate lymphoid cells. Journal of Experimental Medicine, Rockefeller University Press, 2017, 214 (12), pp.3531-3541. ⟨10.1084/jem.20171048⟩. ⟨hal-01764683⟩



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