The spectrum of neuro-immune diseases including: Myalgic Encephalomyelitis (ME/CFS), Atypical MS, Fibromyalgia and Gulf War Syndrome, share common abnormalities in the innate immune response inc, which result in chronic immune activation.
The current working hypothesis is that a viral or environmental trigger in a susceptible host sets up a state of chronic immune activation contributing to alterations of immune responses and resulting in manifestations of disease such as cognitive dysfunction, lymphadenopathy, splenomegaly, chronic pain, inflammation in the tissues and joints and gastrointestinal distress.
It is critical to understand the events that trigger the immune system to become abnormally activated. We are working to understand what these "triggers" are and what the genetic susceptibilities are which render some patients susceptible to that "trigger" while others are relatively resistant.
Neuro Immune Disease related research is active worldwide because the underlying cause of these devastating diseases still remain unknown. Existing treatment strategies are only partially effective, leaving a critical need for new therapies.
Building on previous studies of NK cells by Dr. Nancy Klimas and the RNase L work of Drs. Suhadolnik and Silverman using state of the art technologies, the research program of WPI is addressing fundamental aspects of this hypothesis. We are using an integrated collaborative approach with investigators at the University of Nevada School of Medicine, the National Cancer Institute's cancer inflammation program, the National Institute of Aging, the Nevada Cancer Institute, the Cleveland Clinic and the City of Hope. These studies are yielding new insights into the pathogenesis of this disease.
We have new findings regarding novel viruses in a cohort of Nevada ME/CFS patients with an alarming increase in lymphoma. These findings may have far reaching implications for the prevention and treatment of the lymphoma, one of the potentially devastating complications of ME/CFS.
It has been recognized for more than a decade that pro-inflammatory cytokines are involved in viral persistence by altering the immune response. Our recent findings extend these observations by identifying comprehensive cytokine/chemokine signatures that can be used to develop new treatments and monitor patient responses.