Immunological aspects of chronic fatigue syndrome.
Lorusso, Lorenzo, Mikhaylova, Svetlana V, Capelli, Enrica et al. · Autoimmunity reviews · 2009 · DOI
Quick Summary
This review examines how the immune system may be involved in ME/CFS. Researchers have found that people with ME/CFS often have unusual patterns in immune cells and signaling molecules called cytokines, particularly higher levels of inflammatory markers. These immune system changes might explain some of the main symptoms, like fatigue and flu-like feelings, though the exact role these changes play in causing the disease remains unclear.
Why It Matters
Understanding the immunological basis of ME/CFS is crucial for developing diagnostic tests and targeted treatments. This review consolidates evidence that immune dysfunction is a central feature of the disease, supporting the biological basis of ME/CFS rather than psychological explanations, and may guide future research into immune-modulating therapies.
Observed Findings
Elevated levels of pro-inflammatory cytokines in people with ME/CFS
Decreased natural killer (NK) cell function
Presence of autoantibodies in some patients
Increased CD8+ cytotoxic T lymphocytes with elevated CD38 and HLA-DR activation markers
Abnormal T-cell responses to mitogens and specific antigens
Inferred Conclusions
ME/CFS involves detectable alterations in multiple immune parameters rather than a single immune defect
Pro-inflammatory cytokine elevation may mechanistically contribute to fatigue and flu-like symptoms
ME/CFS pathogenesis is multifactorial, likely involving both immune dysregulation and neuroendocrine disturbances
Abnormal immune activation patterns could reflect an ongoing response to infection or antigen exposure
Remaining Questions
Are immune abnormalities primary drivers of ME/CFS pathogenesis or secondary consequences of the disease process?
Which specific trigger (viral infection, autoimmune response, or other stimulus) initiates the immune dysregulation?
What This Study Does Not Prove
This review does not prove that immune abnormalities cause ME/CFS—these findings may be consequences of the disease rather than triggers. It also does not establish which specific immune dysfunction is primary or sufficient to produce the full clinical syndrome, nor does it validate any single diagnostic immune test for ME/CFS.