Abstract
Post-traumatic stress disorder (PTSD) is a debilitating psychological disorder that increases the risk of comorbid inflammatory diseases by >3 fold, but the mechanisms remain elusive. We previously reported elevated levels of mitochondrial superoxide and inflammatory cytokines in T-lymphocytes from mice undergoing repeated social defeat stress (RSDS; a preclinical model of PTSD). These findings suggested T-lymphocyte activation, but the mechanisms underlying this activation remain elusive. Therefore, we hypothesized that RSDS stimulates antigen presenting cells (i.e., dendritic cells), which in turn potentiates T-lymphocyte activation and pro-inflammatory differentiation.
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