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1 Institute of Medical Microbiology and Hygiene, University of Tübingen, Elfriede-Aulhorn-Straße 6, D-72076 Tübingen, Germany
2 Institute of Microbiology, Czech Academy of Sciences, Videnska 1083, CZ-14220 Prague 4, Czech Republic
Correspondence
Sabine Gröbner
sabine.groebner{at}med.uni-tuebingen.de
Received 8 June 2007
Accepted 23 October 2007
B) activation. However, as shown by measurement of propidium iodide uptake via disrupted cellular membranes, the preincubation of DC with several NF-
B inhibitors prior to infection with Yersinia did not restore the death-inducing capacity of a YopP-deficient Yersinia mutant. These results suggest that in contrast to macrophages, in DC the YopP-dependent inhibition of NF-
B activation is not causative for the induction of cell death. Instead, in DC, the inhibition of mitogen-activated protein kinases (MAPKs), in particular, p38 and c-Jun N-terminal kinase, prior to infection with a YopP-deficient Yersinia mutant substituted the death-inducing capacity of the Yersinia wild-type strain, indicating that the YopP-dependent inhibition of MAPKs mediates Yersinia-induced DC death. The differences between DC and macrophages in the mechanisms of cell death induction by YopP presented herein might be crucial for the function of these antigen-presenting cells.
Abbreviations: CLSM, confocal laser scanning microscopy; DC, dendritic cells; JNK, c-Jun N-terminal kinase; MAPK, mitogen-activated protein kinase; MKK, MAPK kinase; NF-
B, nuclear factor-kappa B; PI, propidium iodide.
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