Altered monocyte activation markers in Tourette’s syndrome: a case–control study
- Equal contributors
1 Department of Psychiatry and Psychotherapy, Ludwig Maximilian University, Nussbaumstr. 7, 80336, Munich, Germany
2 Vinzenz von Paul Hospital, Psychiatry, Schwenninger Str. 55, 78628, Rottweil, Germany
3 Department of Rheumatology, Ludwig Maximilian University, Pettenkoferstr. 8a, 80336, Munich, Germany
BMC Psychiatry 2012, 12:29 doi:10.1186/1471-244X-12-29Published: 2 April 2012
Infections and immunological processes are likely to be involved in the pathogenesis of Tourette’s syndrome (TS). To determine possible common underlying immunological mechanisms, we focused on innate immunity and studied markers of inflammation, monocytes, and monocyte-derived cytokines.
In a cross-sectional study, we used current methods to determine the number of monocytes and levels of C-reactive protein (CRP) in 46 children, adolescents, and adult patients suffering from TS and in 43 healthy controls matched for age and sex. Tumor necrosis factor alpha (TNF-alpha), interleukin 6 (IL-6), soluble CD14 (sCD14), IL1-receptor antagonist (IL1-ra), and serum neopterin were detected by immunoassays.
We found that CRP and neopterin levels and the number of monocytes were significantly higher in TS patients than in healthy controls. Serum concentrations of TNF-alpha, sIL1-ra, and sCD14 were significantly lower in TS patients. All measured values were within normal ranges and often close to detection limits.
The present results point to a monocyte dysregulation in TS. This possible dysbalance in innate immunity could predispose to infections or autoimmune reactions.