4.7 Article

Two Types of Interleukin 17A-Producing γδ T Cells in Protection Against Pulmonary Infection With Klebsiella pneumoniae

期刊

JOURNAL OF INFECTIOUS DISEASES
卷 214, 期 11, 页码 1752-1761

出版社

OXFORD UNIV PRESS INC
DOI: 10.1093/infdis/jiw443

关键词

IL-17A; CD69; IL-23; V gamma 4 gamma delta T cells; V gamma 1(-)V gamma 4(-) gamma delta T cells; Klebsiella pneumoniae

资金

  1. Japan Society for the Promotion of Science [JP 26293098, JP16H06496]
  2. Grants-in-Aid for Scientific Research [16H06496, 15H05787, 26293098] Funding Source: KAKEN

向作者/读者索取更多资源

Background. Klebsiella pneumoniae frequently causes life-threatening infection in children. Interleukin 17A (IL-17A) is known to be involved in protection against K. pneumoniae infection through activation of neutrophils. Methods and Results. We found that IL-17A-producing gamma delta T cells existed more frequently in younger mice on examination of IL-17A-producing lymphocytes in the lung of naive mice at various ages. We hence compared the protective role of IL-17A-producing gamma delta T cells against pulmonary K. pneumoniae infection in young (3 weeks old) and adult (8-12 weeks old) mice. IL-17A-deficient mice were susceptible to K. pneumonia regardless of age. C gamma-, V gamma 4/6-, or V delta 1-deficient mice were susceptible to K. pneumonia at young age, while interleukin 23p19 (IL-23p19)-deficient mice were susceptible at adult age. IL-17A-producing V gamma 1(-)V gamma 4(-) gamma delta T cells expressing canonical V gamma 6/V delta 1 genes were dominant over IL-17A-producing V gamma 4(+) gamma delta T cells in the lungs of young mice after infection. The IL-17A-producing V gamma 1(-)V gamma 4(-) gamma delta T cells expressed an activation marker, CD69, and proliferated in an IL-23-independent manner, while the IL-17A-producing V gamma 4(+) gamma delta T cells expressing IL-23 receptor but no CD69 proliferated in IL-23-dependent manner. Conclusions. These results suggest that 2 types of IL-17A-producing gamma delta T cells are activated for host defense against K. pneumoniae infection by IL-23-dependent or independent mechanism.

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