Neuroimmune Interactions in a Model of Multiple Sclerosis
Psychological stress has been implicated in both the onset and exacerbation of multiple sclerosis (MS). Our research has focused on the role of stress at the onset of MS, using the mouse model Theiler's murine encephalomyelitis virus-induced demyelination. Theiler's virus is a natural pathogen of mice that causes a persistent infection of the central nervous system (CNS) and inflammatory immune-mediated demyelination that is very similar to MS. Our research has shown that restraint stress sufficiently increases corticosterone secretion to cause immunosuppression. Stressed mice develop decreased innate and adaptive immune responses, including decreased chemokine and cytokine responses, to virus, which leads to increased viral replication within the CNS. Higher levels of virus then cause increased later demyelinating disease. These findings may have important implications in our understanding of the interactions between stress and the development of autoimmune diseases induced by infectious agents.
multiple sclerosis stress demyelination theiler's virus central nervous system restraint stress corticosterone adaptive immunity chemokines cytokines autoimmunity viruses glucocorticoids hpa axis immune system nk cells interferon macrophages innate immunity th1 th2 t cells cd4+ t cells cd8+ t cells inflammation