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Cell Microbiol. 2018 Jul;20(7):e12833. doi: 10.1111/cmi.12833. Epub 2018 Mar 9.

NK cells inhibit anti-Mycobacterium bovis BCG T cell responses and aggravate pulmonary inflammation in a direct lung infection mouse model.

Wang D1,2, Gu X1,2, Liu X1, Wei S1, Wang B1,2, Fang M1,3.

Author information

1
CAS Key Laboratory of Pathogenic Microbiology and Immunology, Institute of Microbiology, Chinese Academy of Sciences, Beijing, China.
2
University of Chinese Academy of Sciences, Beijing, China.
3
International College, University of Chinese Academy of Sciences, Beijing, China.

Abstract

Tuberculosis remains a threat to public health. The major problem for curing this disease is latent infection, of which the underlying mechanisms are still not fully understood. Previous studies indicate that natural killer (NK) cells do not play a role in inhibiting the growth of Mycobacterium tuberculosis in the lung, and recent studies have revealed that NK cells regulate the adaptive immunity during mycobacterial infection. By using a mouse model of direct lung infection with Mycobacterium bovis bacillus Calmette-Guerin (BCG), we found that the presence of NK cells postponed the priming and activation of T cells after BCG infection. In addition, depletion of NK cells before infection alleviated pulmonary pathology. Further studies showed that NK cells lysed BCG-infected macrophages in an NKG2D dependent manner. Thus, NK cells did not play a direct role in control BCG, but aggravated the pulmonary inflammation and impaired anti-BCG T cell immunity, likely through killing BCG-infected macrophages. Our results may have important implications for the design of immune therapy to treat tuberculosis.

KEYWORDS:

BCG; NK cells; NKG2D; T cell responses; pulmonary pathology

PMID:
29447423
DOI:
10.1111/cmi.12833
[Indexed for MEDLINE]

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