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¹ Division of Infectious Diseases, Department of Medicine, ² Department of Pathology, and ³ Department of Microbiology, New York University School of Medicine, New York, NY 10016
⁴ Biomedical Sciences Graduate Program, University of California, San Francisco, CA 94143
⁵ Department of Microbiology, Leprosy Research Center, National Institute of Infectious Disease, Tokyo 189-0002, Japan
⁶ Department of Microbiology and Immunology, Division of Immunology, The Institute of Medical Science, The University of Tokyo, Tokyo 108-8639, Japan
⁷ Department of Pathology, Stanford University School of Medicine, Palo Alto, CA 94305

CORRESPONDENCE Joel D. Ernst: joel.ernst{at}med.nyu.edu OR Kiyoshi Takatsu: takatsuk{at}ims.u-tokyo.ac.jp

The onset of the adaptive immune response to Mycobacterium tuberculosis is delayed compared with that of other infections or immunization, and allows the bacterial population in the lungs to expand markedly during the preimmune phase of infection. We used adoptive transfer of M. tuberculosis Ag85B-specific CD4⁺ T cells to determine that the delayed adaptive response is caused by a delay in initial activation of CD4⁺ T cells, which occurs earliest in the local lung-draining mediastinal lymph node. We also found that initial activation of Ag85B-specific T cells depends on production of antigen by bacteria in the lymph node, despite the presence of 100-fold more bacteria in the lungs. Although dendritic cells have been found to transport M. tuberculosis from the lungs to the local lymph node, airway administration of LPS did not accelerate transport of bacteria to the lymph node and did not accelerate activation of Ag85B-specific T cells. These results indicate that delayed initial activation of CD4⁺ T cells in tuberculosis is caused by the presence of the bacteria in a compartment that cannot be mobilized from the lungs to the lymph node, where initial T cell activation occurs.

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