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Increased soluble interleukin-2 receptor levels are related to somatic but not to cognitive-affective features in major depression
Authors:Frank Euteneuer  Markus J Schwarz  Katharina Dannehl  Anja Hartung  Stefan Westermann  Winfried Rief
Institution:1. Department of Neurology, St. Josef-Hospital, Ruhr-University Bochum, Gudrunstr. 56, 44791 Bochum, Germany;2. Department of Molecular and Medical Virology, Ruhr-University Bochum, Universitätsstr. 150, 44801 Bochum, Germany;3. Department of Dermatology, St. Josef-Hospital, Ruhr-University Bochum, Gudrunstr. 56, 44791 Bochum, Germany;4. Institute of Molecular Virology, Ulm University, Meyerhofstr. 1, 89081 Ulm, Germany;5. Department of Neurosurgery, University Duisburg-Essen, Hufelandstr. 55, 45147 Essen, Germany;6. Institute of Clinical and Molecular Virology, University Erlangen, Schloßgarten 4, 91054 Erlangen, Germany;7. Fraunhofer Institute for Cell Therapy and Immunology, Perlickstr. 1, 04103 Leipzig, Germany
Abstract:Cell-mediated immune activation may play a role in the pathogenesis of depression as indicated by findings of increased soluble tumor necrosis factor receptor (sTNF-R) levels and meta-analytic evidence for elevated soluble interleukin-2 receptor (sIL-2R) concentrations. However, little research has been done on how these soluble cytokine receptors are differently related to specific features in patients with depression. We measured levels of the soluble cytokine receptors sIL-2R, sTNF-R1 and sTNF-R2 in 25 non-medicated patients with major depression (DSM-IV) and 22 healthy controls. Psychometric measures included cognitive-affective depressive symptoms, somatoform symptoms, somatic and cognitive dimensions of anxiety and current mood states. While patients with depression showed increased levels of sIL-2R (p < 0.01), differences in sTNF-R1 (p = 0.09) and sTNF-R2 (p = 0.08) marginally failed to reach significance. Increased concentrations of sIL-2R were related to somatic measures such as the severity of somatoform symptoms and somatic anxiety symptoms but not to cognitive-affective measures or current mood states. Our findings may suggest some specificity in the relationship between sIL-2R and symptom dimensions and highlight potential pathways by which T cell mediated immune activation may underpin somatic symptoms in depression.
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