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-γ production, thereby al

SUBMITTER: Quatrini L 

PROVIDER: S-EPMC5716043 | biostudies-literature | 2017 Dec

REPOSITORIES: biostudies-literature