The Journal of Experimental Medicine
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Published online
doi:10.1084/jem.20062105
The Journal of Experimental Medicine, Vol. 204, No. 9, 2159-2169
The Rockefeller University Press, 0022-1007 $30.00
© Scott-Browne et al.
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Article

 Expansion and function of Foxp3-expressing T regulatory cells during tuberculosis

James P. Scott-Browne1, Shahin Shafiani1, Glady's Tucker-Heard1, Kumiko Ishida-Tsubota1, Jason D. Fontenot2, Alexander Y. Rudensky2,3, Michael J. Bevan2,3, and Kevin B. Urdahl1,2

1 Department of Pediatrics, 2 Department of Immunology, and 3 Howard Hughes Medical Institute, University of Washington, Seattle, WA 98195

CORRESPONDENCE Kevin B. Urdahl:kurdah{at}u.washington.edu

Mycobacterium tuberculosis (Mtb) frequently establishes persistent infections that may be facilitated by mechanisms that dampen immunity. T regulatory (T reg) cells, a subset of CD4+ T cells that are essential for preventing autoimmunity, can also suppress antimicrobial immune responses. We use Foxp3-GFP mice to track the activity of T reg cells after aerosol infection with Mtb. We report that during tuberculosis, T reg cells proliferate in the pulmonary lymph nodes (pLNs), change their cell surface phenotype, and accumulate in the pLNs and lung at a rate parallel to the accumulation of effector T cells. In the Mtb-infected lung, T reg cells accumulate in high numbers in all sites where CD4+ T cells are found, including perivascular/peribronchiolar regions and within lymphoid aggregates of granulomas. To determine the role of T reg cells in the immune response to tuberculosis, we generated mixed bone marrow chimeric mice in which all cells capable of expressing Foxp3 expressed Thy1.1. When T reg cells were depleted by administration of anti-Thy1.1 before aerosol infection with Mtb, we observed ~1 log less of colony-forming units of Mtb in the lungs. Thus, after aerosol infection, T reg cells proliferate and accumulate at sites of infection, and have the capacity to suppress immune responses that contribute to the control of Mtb.

Abbreviations used: ICOS, inducible costimulatory molecule; mLN, mesenteric LN; Mtb, Mycobacterium tuberculosis; pLN, pulmonary lymph node; RFP, red fluorescent protein.

J.P. Scott-Browne's present address is Integrated Dept. of Immunology, University of Colorado Health Sciences Center, National Jewish Medical Research Center, Denver, CO 80209.

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