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CUTTING EDGE |
* Department of Immunology, Max Planck Institute for Infection Biology, Berlin, Germany;
Institut für Immunologie, Klinikum der Friedrich-Schiller-Universität Jena, Jena, Germany; and
Institute for Immunology, University Medical Center Hamburg-Eppendorf, Hamburg, Germany
Mycobacterium tuberculosis remains one of the top microbial killers of humans causing 
2 million deaths annually. More than 90% of the 2 billion individuals infected never develop active disease, indicating that the immune system is able to generate mechanisms that control infection. However, the immune response generally fails to achieve sterile clearance of bacilli. Using adoptive cell transfer into C57BL/6J-Rag1tm1Mom mice (Rag1–/–), we show that regulatory T cells prevent eradication of tubercle bacilli by suppressing an otherwise efficient CD4+ T cell response. This protective CD4+ T cell response was not correlated with increased numbers of IFN-
- or TNF-
-expressing cells or general expression levels of IFN- or inducible NO synthase in infected organs compared with wild-type C57BL/6 animals. Furthermore, suppression of protection by cotransferred regulatory T cells was neither accompanied by a general increase of IL-10 expression nor by higher numbers of IL-10-producing CD4+ T cells.
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 Address correspondence and reprint requests to Dr. Mischo Kursar, Max Planck Institute for Infection Biology, Charitéplatz 1, 10117 Berlin, Germany. E-mail address: kursar{at}mpiib-berlin.mpg.de
2 Mi.K. and Ma.K. contributed equally to this work.
3 Abbreviations used in this paper: Treg, regulatory T cell; fw, forward; rev, reverse; iNOS, inducible NO synthase; wt, wild type.
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