Journal articles
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.
Cited literature [54 references]
https://hal-amu.archives-ouvertes.fr/hal-01764683
Contributor : Carine Dou Goarin <>
Submitted on : Friday, April 13, 2018 - 11:08:39 AM
Last modification on : Tuesday, May 26, 2020 - 6:50:50 PM
Contributor : Carine Dou Goarin <>
Submitted on : Friday, April 13, 2018 - 11:08:39 AM
Last modification on : Tuesday, May 26, 2020 - 6:50:50 PM
File
3531.full.pdf
Publisher files allowed on an open archive