The Journal of Experimental Medicine
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Published online 14 October 2002 doi:10.1084/jem.20020908
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© Rockefeller University Press, 0022-1007/2002/10/1017 $5.00
The Journal of Experimental Medicine, Volume 196, Number 8, 1017-1024

Yersinia V–Antigen Exploits Toll-like Receptor 2 and CD14 for Interleukin 10–mediated Immunosuppression

Andreas Sing1, Dagmar Rost1, Natalia Tvardovskaia1, Andreas Roggenkamp1, Agnès Wiedemann1, Carsten J. Kirschning2, Martin Aepfelbacher1 and Jürgen Heesemann1

1 Max von Pettenkofer-Institut für Hygiene und Medizinische Mikrobiologie, Ludwig-Maximilians-Universität München, Pettenkoferstrasse 9a, 80336 München, Germany
2 Institut für Medizinische Mikrobiologie, Immunologie und Hygiene, Technische Universität München, Trogerstrasse 32, 81675 München, Germany

Address correspondence to Jürgen Heesemann, Max von Pettenkofer-Institut für Hygiene und Medizinische Mikrobiologie, Pettenkoferstrasse 9a, 80336 München, Germany. Phone: 49-89-5160-5200; Fax: 49-89-5160-5202; E-mail: heesemann{at}m3401.mpk.med.uni-muenchen.de

A characteristic of the three human-pathogenic Yersinia spp. (the plague agent Yersinia pestis and the enteropathogenic Yersinia pseudotuberculosis and Yersinia enterocolitica) is the expression of the virulence (V)-antigen (LcrV). LcrV is a released protein which is involved in contact-induced secretion of yersinia antihost proteins and in evasion of the host's innate immune response. Here we report that recombinant LcrV signals in a CD14- and toll-like receptor 2 (TLR2)-dependent fashion leading to immunosuppression by interleukin 10 induction. The impact of this immunosuppressive effect for yersinia pathogenesis is underlined by the observation that TLR2-deficient mice are less susceptible to oral Y. enterocolitica infection than isogenic wild-type animals. In summary, these data demonstrate a new ligand specificity of TLR2, as LcrV is the first known secreted and nonlipidated virulence-associated protein of a Gram-negative bacterium using TLR2 for cell activation. We conclude that yersiniae might exploit host innate pattern recognition molecules and defense mechanisms to evade the host immune response.

Key Words: immunity • monocytes/macrophages • inflammation • bacterial proteins • immunosuppression


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