Quick Search:

uzh logo
Browse by:

Zurich Open Repository and Archive 

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.

[img] 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 16:20
Last Modified:27 Nov 2013 23:40
Publisher DOI:10.1016/j.bbi.2010.11.001
PubMed ID:21074606
Citations:Web of Science®. Times Cited: 7
Google Scholar™
Scopus®. Citation Count: 6

Users (please log in): suggest update or correction for this item

Repository Staff Only: item control page