Immune System Dysfunction May Play A Key Role.(in the cause of chronic fatigue syndrome)

2002 JAN 17 - (NewsRx.com & NewsRx.net) -- Research on the immune system could shed light on the cause of chronic fatigue syndrome (CFS), including whether a pathogenic agent such as a virus or bacteria is involved.

This was one conclusion reached by a panel of experts that convened in October 2001 for the third in a series of scientific symposia on CFS. The symposium was sponsored by The Chronic Fatigue and Immune Dysfunction Syndrome (CFIDS) Association of America, the U.S. Centers for Disease Control and Prevention (CDC), and the National Institutes of Health Office of Research on Women's Health (ORWH).

A number of studies have suggested involvement of the immune system in CFS. New findings include the discovery of autoantibodies in CFS patients, which has led to increased speculation that the illness may be an autoimmune disorder. Because many cases of CFS begin with a flu or mono-like illness, viruses, bacteria, and toxins have also been studied as possible causes.

"The immune system may provide important clues to CFS, but it cannot be studied in isolation," said Kimberly Kenney, of The CFIDS Association of America. "A new emphasis on multidisciplinary research to explore links between the immune, neuroendocrine, and cardiovascular systems in CFS is crucial to developing a better understanding of this complex illness."

Following a day of presentations by experts from around the world, an independent panel composed of researchers and practitioners in many fields, including biostatistics, endocrinology, immunology, infectious disease, internal medicine, microbiology, psychiatry, and rheumatology, developed a statement on the key issues surrounding the role of the immune system in CFS.

The panel agreed that:

* The immune system is involved in CFS. There has been substantial published evidence that a large proportion of CFS patients have immunological abnormalities, including increased natural killer cell activity, increased number or activated T cells, decreased lymphocyte stimulation and increased production of some pro-inflammatory cytokines, which act as chemical messengers between cells. The panel noted that the ability to understand the exact role these changes play in the development of CFS is constrained by major limitations in the studies conducted to date.