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Published on: November 27, 2014
Cellular and humoral immune abnormalities in Gulf War veterans
Aristo Vojdani1, Jack D Thrasher
1Section of Neuroimmunology, Immunosciences Lab Inc., 8693 Wilshire Boulevard, Suite 200, Beverly Hills, CA 90211, USA. drari@msn.com
Insights
Gulf War veterans show significant immune system alterations, including elevated B cells and immune complexes, and decreased natural killer cell activity, years after service. These changes suggest Gulf War syndrome is a complex illness linked to environmental exposures.
Area of Science:
- Immunology
- Environmental Medicine
- Veterans' Health
Background:
- Gulf War syndrome (GWS) is a complex, multi-symptom illness affecting veterans.
- The underlying pathophysiology of GWS remains incompletely understood, with potential links to environmental exposures during deployment.
Purpose of the Study:
- To investigate immunologic differences between symptomatic Gulf War veterans and controls.
- To identify specific immune markers associated with Gulf War service.
Main Methods:
- Compared 100 symptomatic Gulf War veterans with 100 controls.
- Assessed T cell percentages (CD3), B cell percentages (CD19), CD4:CD8 ratio, natural killer (NK) cell activity, mitogenic responses (PHA, PWM), immune complexes, autoantibodies (MBP, muscle), and viral antibodies (EBV, CMV, HSV-1, HSV-2, HHV-6, VZV).
Main Results:
- Elevated B cell percentages and immune complexes in veterans.
- Significantly decreased NK cell activity and altered mitogenic responses in veterans.
- Increased autoantibodies and viral antibodies in veterans compared to controls.
- Immune alterations persisted 2-8 years post-deployment.
Conclusions:
- Gulf War veterans exhibit significant immune system dysregulation.
- These immune alterations are consistent with exposure to environmental factors.
- Gulf War syndrome is a multifaceted illness with immune dysfunction potentially linked to chronic fatigue syndrome.
Abstract:
We examined 100 symptomatic Gulf War veterans (patients) and 100 controls for immunologic assays. The veterans and controls were compared for the percentage of T cells (CD3); B cells (CD19); helper:suppressor (CD4:CD8) ratio; natural killer (NK) cell activity; mitogenic response to phytohemagglutin (PHA) and pokeweed mitogen (PWM); level of immune complexes; myelin basic protein (MBP) and striated and smooth muscle autoantibodies; and antibodies against Epstein-Barr virus, cytomegalovirus, herpes simplex virus type 1 (HSV-1), HSV-2, human herpes Type 6 (HHV-6), and Varicella zoster virus (VZV). The percentage of T cells in patients versus controls was not significantly different, whereas a significantly higher proportion of patients had elevated T cells compared with controls. The percentage of B cells was significantly elevated in the patients versus the controls. The NK cell (NK) activity was significantly decreased in the patients (24.8 +/- 16.5 lytic units) versus the controls (37.3 +/- 26.4 lytic units). The percentage of patients with lower than normal response to PHA and PWM was significantly different from controls. Immune complexes were significantly increased in the patients (53.1 +/- 18.6, mean +/- SD) versus controls (34.6 +/- 14.3). Autoantibody titers directed against MBP and striated or smooth muscle were significantly greater in patients versus controls. Finally, the patients had significantly greater titers of antibodies to the viruses compared with the controls (p < 0.001). These immune alterations were detected 2-8 years after participation in the Gulf War. The immune alterations are consistent with exposure to different environmental factors. We conclude that Gulf War syndrome is a multifaceted illness with immune function alterations that may be induced by various factors and are probably associated with chronic fatigue syndrome.
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