TNFR1 is essential for CD40, but not for lipopolysaccharide-induced sickness behavior and clock gene dysregulation

Taraborrelli, Cornelia; Palchykova, Svitlana; Tobler, Irene; Gast, Heidemarie; Birchler, Thomas; Fontana, Adriano (2011). TNFR1 is essential for CD40, but not for lipopolysaccharide-induced sickness behavior and clock gene dysregulation. Brain, behavior, and immunity, 25(3), pp. 434-42. Amsterdam: Elsevier 10.1016/j.bbi.2010.11.001

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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 (Original Article)

Division/Institute:

04 Faculty of Medicine > Department of Head Organs and Neurology (DKNS) > Clinic of Neurology

UniBE Contributor:

Palchykova, Svitlana and Gast, Heidemarie

Subjects:

600 Technology > 610 Medicine & health

ISSN:

0889-1591

Publisher:

Elsevier

Funders:

[4] Swiss National Science Foundation
[7] Swiss Multiple Sclerosis Society

Language:

English

Submitter:

Factscience Import

Date Deposited:

04 Oct 2013 14:14

Last Modified:

20 Dec 2014 17:42

Publisher DOI:

10.1016/j.bbi.2010.11.001

PubMed ID:

21074606

Web of Science ID:

000287626600009

BORIS DOI:

10.7892/boris.3357

URI:

https://boris.unibe.ch/id/eprint/3357 (FactScience: 207018)

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