Permanent URL to this publication: http://dx.doi.org/10.5167/uzh-46693
Taraborrelli, C; Palchykova, S; Tobler, I; Gast, H; Birchler, T; Fontana, A (2011). TNFR1 is essential for CD40, but not for lipopolysaccharide-induced sickness behavior and clock gene dysregulation. Brain, Behavior, and Immunity, 25(3):434-442.
|PDF - Registered users only|
Autoimmune and infectious diseases are associated with behavioral changes referred to as sickness behavior syndrome (SBS). In autoimmunity, the generation of anti-self T lymphocytes and autoantibodies critically involves binding of CD40 ligand on T-cells to its receptor CD40 on B-cells, dendritic cells and macrophages. Activation of CD40 leads to production of proinflammatory cytokines and, as shown here, induces SBS. Here we report that these behavioral changes depend on the expression of tumor necrosis factor alpha receptor 1 (TNFR1), but not on interleukin-1 receptor 1 or interleukin-6. Moreover, the intensity of SBS correlates with suppression of E-box controlled clock genes, including Dbp, and upregulation of Bmal1. However, the absence of TNFR1 does not interfere with the development of SBS and dysregulation of clock genes in mice treated with lipopolysaccharide. Thus, our results suggest that TNFR1 mediates SBS and dysregulation of clock genes in autoimmune diseases.
|Item Type:||Journal Article, refereed, original work|
|Communities & Collections:||04 Faculty of Medicine > University Hospital Zurich > Clinic for Immunology|
04 Faculty of Medicine > University Hospital Zurich > Institute of Experimental Immunology
|DDC:||570 Life sciences; biology|
610 Medicine & health
|Deposited On:||08 Mar 2011 17:20|
|Last Modified:||23 Nov 2012 16:45|
Users (please log in): suggest update or correction for this item
Repository Staff Only: item control page