Chronicle Issues
  Research Review Issues
  CFIDSLink
E-newsletter
  Reprint Policies

RETURN TO TABLE OF CONTENTS
Winter 2002

Symposium Panel Concurs: Immune System Involved in CFIDS

Research on the immune system could shed light on the cause of chronic fatigue and immune dysfunction syndrome (CFIDS) — 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 last fall for the third in a series of scientific symposia on CFIDS.

The symposium was sponsored by The CFIDS Association of America, the U.S. Centers for Disease Control and Prevention and the National Institutes of Health Office of Research on Women’s Health.

A number of studies have suggested that the immune system may play a role in CFIDS, which is also known as chronic fatigue syndrome (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 Association President & CEO Kim Kenney. “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. Substantial published evidence shows that many CFS patients have immunological abnormalities, including increased natural killer cell activity, increased number of 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.
  • Infections may also play a role. The panel concluded that direct and indirect evidence points to the involvement of active viral or bacterial infections in the development of some cases of CFS, although no single agent has been found in all patients.
  • CFS is a multisystem disorder. In addition to the immune system, the endocrine and autonomic nervous systems may be implicated in CFS. The panel acknowledged that little is known about the influence of any of these systems in individuals with the illness.
  • More research is needed to define the immunological aspects of CFS. The panel outlined future research needs, including multiple site, longitudinal studies to: explore the possible association of infectious agents with the immunological profile seen in CFS; link immunological findings to symptoms and functional disability; and explore the use of anti-inflammatory cytokines, antivirals, antibiotics and immunomodulatory agents in the treatment of CFS.

The CFS assessment symposia series is designed to examine the role of the neurological, endocrine, circulatory and immune systems in CFS. The symposia gather experts to evaluate research findings, identify promising next steps for research, define research and funding priorities and create collaborative research teams.