Ontology highlight
ABSTRACT: Background
Post-traumatic stress disorder (PTSD) is a debilitating psychological disorder that also presents with neuroimmune irregularities. Patients display elevated sympathetic tone and are at an increased risk of developing secondary autoimmune diseases. Previously, using a mouse model of repeated social defeat stress (RSDS) that recapitulates certain features of PTSD, we demonstrated that elimination of sympathetic signaling to T-lymphocytes specifically limited their ability to produce pro-inflammatory interleukin 17A (IL-17A); a cytokine implicated in the development of many autoimmune disorders. However, the mechanism linking sympathetic signaling to T-lymphocyte IL-17A production remained unclear.Methods
Using a modified version of RSDS that allows for both males a
SUBMITTER: Lauten TH
PROVIDER: S-EPMC11967417 | biostudies-literature | 2025 Jan
REPOSITORIES: biostudies-literature