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J. Biol. Chem., Vol. 283, Issue 10, 6438-6448, March 7, 2008

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Reduced Display of Tumor Necrosis Factor Receptor I at the Host Cell Surface Supports Infection with Chlamydia trachomatis^*

Nicole Paland, Linda Böhme, Rajendra Kumar Gurumurthy, André Mäurer, Agnes J. Szczepek, and Thomas Rudel¹

From the Research Group for Molecular Infection and Tumor Biology, the Department of Molecular Biology, Max Planck Institute for Infection Biology, Charitéplatz 1, D-10117 Berlin, Germany

The obligate intracellular human pathogenic bacterium Chlamydia trachomatis has evolved multiple mechanisms to circumvent the host immune system. Infected cells exhibit a profound resistance to the induction of apoptosis and down-regulate the expression of major histocompatibility complex class I and class II molecules to evade the cytotoxic effect of effector immune cells. Here we demonstrate the down-regulation of tumor necrosis factor receptor 1 (TNFR1) on the surface of infected cells. Interestingly, other members of the TNFR family such as TNFR2 and CD95 (Fas/Apo-1) were not modulated during infection, suggesting a selective mechanism underlying surface reduction of TNFR1. The observed effect was not due to reduced expression since the overall amount of TNFR1 protein was increased in infected cells. TNFR1 accumulated at the chlamydial inclusion and was shed by the infected cell into the culture supernatant. Receptor shedding depended on the infection-induced activation of the MEK-ERK pathway and the metalloproteinase TACE (TNF converting enzyme). Our results point to a new function of TNFR1 modulation by C. trachomatis in controlling inflammatory signals during infection.

Received for publication, October 10, 2007 , and in revised form, December 20, 2007.

^* This work was supported by Grant DFG SPP1130 and funding under the Sixth Research Framework Programme of the European Union, Project RIGHT (LSHB-CT-2004 005276) (to T. R.). The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

¹ To whom correspondence should be addressed: Dept. of Molecular Biology, Max Planck Institute for Infection Biology, Charitéplatz 1, D-10117 Berlin, Germany. Tel.: 49-30-28460-415; Fax: 49-30-28460-401; E-mail: rudel{at}mpiib-berlin.mpg.de.

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