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14 NK T cells in Mycobacterium bovis Bacillus Calmette-Guérin-Infected Mice1
* Department of Biopathology, University of Palermo, Palermo, Italy;
Division of Molecular Immunology, Center for Biomedical Science, Chiba University School of Medicine, Chiba, Japan;
La Jolla Institute for Allergy and Immunology, San Diego, CA 92121;
King’s College London at Guy’s Dental and Medical School, London, United Kingdom;
¶ Laboratory of Bacteriology and Clinical Mycology, National Institute of Health, Rome, Italy; and
|| Institute of Advanced Diagnostic Methodologies, National Research Council, Palermo, Italy
The possible contribution of NKT cells to resistance to Mycobacterium tuberculosis infection remains unclear. In this paper we characterized the V
14 NKT cell population following infection with Mycobacterium bovis bacillus Calmette-Guérin (BCG). BCG infection determined an early expansion of V14 NKT cells in liver, lungs, and spleen, which peaked on day 8 and was sustained until day 30. However, an NK1.1+ V14 NKT population preferentially producing IFN-
predominated at an early stage (day 8), which was substituted by an NK1.1- population preferentially producing IL-4 at later stages (day 30). Despite the fact that V14 NKT cell-deficient mice eliminated BCG as did control mice, they had significantly higher numbers of granulomas in liver and lungs. Additionally, while control mice developed organized small granulomas, those in V14 NKT-deficient mice had signs of caseation, large cellular infiltrates, and some multinucleated macrophages, suggesting that V14 NKT cells may actually work as anti-inflammatory cells by limiting excessive lymphocyte influx and tissue pathology. In agreement, we found an increased spontaneous production and mRNA expression of TNF- in liver and lungs of V14 NKT-deficient mice, whose neutralization in vivo by anti-TNF- mAbs consistently reduced the number of granulomas in liver and lungs. Together, our results support a regulatory role for V14 NKT cells in the course of BCG infection through their ability to limit the extent of inflammatory response and point to an important role for this cell subset as a regulator of the balance between protective responses and immunopathology.
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