Immune activation and depression in women with rheumatoid arthritis

OBJECTIVE: We examined markers of immune activation during periods of stress and depressive symptoms in 45 female patients with rheumatoid arthritis (RA) in comparison to 106 controls with no autoimmune disease. METHODS: Depressive symptoms were recorded, clinician ratings of disease activity were m...

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Bibliographic Details
Published in:Journal of rheumatology 2004-03, Vol.31 (3), p.457-463
Main Authors: ZAUTRA, Alex J, YOCUM, David C, VILLANUEVA, Isidro, SMITH, Bruce, DAVIS, Mary C, ATTREP, Jeanne, IRWIN, Michael
Format: Article
Language:English
Subjects:
Aged
Arthritis, Rheumatoid - immunology
Arthritis, Rheumatoid - psychology
Biological and medical sciences
Biomarkers
Depression - immunology
Diseases of the osteoarticular system
Female
Humans
Inflammatory joint diseases
Interleukin-6 - biosynthesis
Medical sciences
Middle Aged
Stress, Psychological - immunology
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Summary:OBJECTIVE: We examined markers of immune activation during periods of stress and depressive symptoms in 45 female patients with rheumatoid arthritis (RA) in comparison to 106 controls with no autoimmune disease. METHODS: Depressive symptoms were recorded, clinician ratings of disease activity were made, and blood was drawn for RA patients and controls at baseline and during a designated stressful week. RESULTS: Counts of T cell subpopulations revealed significant differences between RA and control groups in proportions of CD8 and CD4 cells, with higher CD4 and lower CD8 counts for the RA participants. Significant depression by diagnosis interactions were found, revealing greater CD4 activation among RA patients who were depressed in comparison to other groups. Only marginally significant effects of stress were found on T cell counts. Interleukin 6 (IL-6) concentrations also differentiated groups, with the highest levels of IL-6 observed for depressed RA patients under stress. CONCLUSION: These findings provide new evidence that psychosocial factors play a significant role in autoimmune processes that underlie RA.
ISSN:0315-162X
1499-2752