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ler
,
Divisions of
*
Hematology and Oncology and
Dermatology, Department of Medicine, and
Department of Microbiology and Immunology, University of California, Los Angeles, School of Medicine, Los Angeles, CA 90095;
Institut für Klinische Mikrobiologie, Immunologie und Hygiene, Friedrich-Alexander Universität Erlangen-Nürnberg, Erlangen, Germany;
¶
Department of Pediatrics, Stanford University, Stanford, CA 94305; and
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Department of Microbiology and Immunology, Albert Einstein College of Medicine, Bronx, NY 10461
Human NKT cells are a unique subset of T cells that express an invariant V
24 TCR that recognizes the nonclassical Ag-presenting molecule CD1d. Activation of NKT cells is greatly augmented by the marine sponge-derived glycolipid -galactosylceramide (GalCer). Because human monocyte-derived cells express CD1d and can harbor the intracellular pathogen Mycobacterium tuberculosis, we asked whether the addition of GalCer could be used to induce effector functions of NKT cells against infected monocytes, macrophages, and monocyte-derived dendritic cells. NKT cells secreted IFN-
, proliferated, and exerted lytic activity in response to GalCer-pulsed monocyte-derived cells. Importantly, GalCer-activated NKT cells restricted the growth of intracellular M. tuberculosis in a CD1d-dependent manner. NKT cells that exhibited antimycobacterial activity also expressed granulysin, an antimicrobial peptide shown to mediate an antimycobacterial activity through perturbation of the mycobacterial surface. Degranulation of NKT cells resulted in depletion of granulysin and abrogation of antimycobacterial activity. The detection of CD1d in granulomas of tuberculosis patients supports the potential interaction of NKT cells with CD1d-expressing cells at the site of disease activity. These studies provide evidence that GalCer-activated CD1d-restricted T cells can participate in human host defense against M. tuberculosis infection.
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