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International Immunology, Vol. 16, No. 3, pp. 415-421, March 2004
© 2004 Japanese Society for Immunology

FAST TRACK

Protective T cell response against intracellular pathogens in the absence of Toll-like receptor signaling via myeloid differentiation factor 88

Mischo Kursar1, Hans-Willi Mittrücker1, Markus Koch1, Anne Köhler1, Marion Herma1 and Stefan H. E. Kaufmann1

1 Department of Immunology, Max-Planck-Institute for Infection Biology, Schumannstrasse 21/22, 10117 Berlin, Germany

The first two authors contributed equally to this work
Correspondence to: H.-W. Mittrücker; E-mail: mittruecker{at}mpiib-berlin.mpg.de
Transmitting editor: S. Akira

Toll-like receptors (TLR) have been indicated as germline-encoded receptors for sensing a variety of pathogens. Although the role of TLR in innate immunity is beyond question, their function in acquired immunity, in particular in T cell immunity, is less clear. Here, we used experimental Listeria monocytogenes infection of mice to analyze requirements for TLR2, TLR4 and the central TLR adaptor protein myeloid differentiation factor 88 (MyD88) in the generation of specific T cell responses. We demonstrate that following L. monocytogenes infection, mice deficient in TLR2, TLR4 and MyD88 can generate Listeria-specific CD8+ and CD4+ Th1 responses. These T cell responses are sufficient to control secondary infection with a high dose of L. monocytogenes even in the absence of TLR signaling via MyD88. Thus, TLR2-, TLR4- and MyD88-dependent signals are not essential for the generation of CD4+ Th1 and CD8+ T cells, and T cells can protect mice against infection in the absence of these signals.

Keywords: bacterial infection, Listeria monocytogenes, T cell, Toll-like receptor activation


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