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International Immunology Advance Access originally published online on May 21, 2009
International Immunology 2009 21(7):779-791; doi:10.1093/intimm/dxp046
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© The Japanese Society for Immunology. 2009. All rights reserved. For permissions, please e-mail: journals.permissions@oxfordjournals.org

Functionally relevant decreases in activatory receptor expression on NK cells are associated with pulmonary tuberculosis in vivo and persist after successful treatment

Federica Bozzano1, Paola Costa2, Giovanni Passalacqua3,4, Ferdinando Dodi5, Silvia Ravera3,4, Gabriella Pagano5, Giorgio W. Canonica3,4, Lorenzo Moretta1,2,6 and Andrea De Maria1,3,7

1 Centro di Eccellenza per la Ricerca Biomedica, Università di Genova, Genova, Italy
2 Istituto G. Gaslini, Genova, Italy
3 Dipartimento di Medicina Interna
4 Clinica Pneumologica e Tisiologica, Università di Genova, Genova, Italy
5 U.O.C. Malattie Infettive, Ospedale San Martino, Genova, Italy
6 Dipartimento di Medicina Sperimentale, Università di Genova, Genova, Italy
7 S.S. Infettivologia, Istituto Nazionale per la Ricerca sul Cancro, Largo Rosanna Benzi 10, 16132 Genova, Italy

Correspondence to: A. De Maria; E-mail: de-maria{at}unige.it

Correlates for the initiation of Mycobacterium tuberculosis hominis (Mth) replication from latency are needed in order to improve Mth control. In order to analyze if perturbations of peripheral NK cells may be associated with exit from Mth latency, sequential patients with newly diagnosed lung tuberculosis (TB) were studied. Peripheral NK cells were analyzed by cytofluorometry, in vitro culture and functional assays. At the onset of lung TB, imbalances in NK cell subsets were evident. Decreased CD56brightCD16+/– subsets with significantly compromised NKp30 and NKp46 expression and with specifically decreased {gamma}-IFN production upon triggering were evident. These features were not completely restored when purified NK cells were cultured in vitro. Culture supplementation with {alpha}-IFN increased only NKp30 expression in TB and healthy donors. Extensive peripheral NK cell triggering was evident in these patients, as shown by the expression of NK cell activation markers and of the lymph node-homing chemokine receptor CCR7 on CD16+ CD56dull cells. Significant persistence of decreased NKp30 and NKp46 after successful treatment with a standard four-drug regimen was detected after full recovery. NK cell function is deeply affected in patients at the onset of pulmonary TB. The involvement of multiple activatory receptors may provide a relevant contribution to the spread of mycobacteria exiting from latency.

Keywords: {alpha}-IFN, immunoreconstitution, latency, Mth, NK cells, pulmonary tuberculosis

Transmitting editor: E. Vivier

Received 26 December 2008, accepted 20 April 2009.


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