title: Two Types of Interleukin 17A-Producing γδ T Cells in Protection Against Pulmonary Infection With Klebsiella pneumoniae.
abstract: 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.
  
  
  RESULTS
  We found that IL-17A-producing γδ 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 γδ 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. Cγ-, Vγ4/6-, or Vδ1-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 Vγ1-Vγ4-γδ T cells expressing canonical Vγ6/Vδ1 genes were dominant over IL-17A-producing Vγ4+γδ T cells in the lungs of young mice after infection. The IL-17A-producing Vγ1-Vγ4-γδ T cells expressed an activation marker, CD69, and proliferated in an IL-23-independent manner, while the IL-17A-producing Vγ4+γδ 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 γδ T cells are activated for host defense against K. pneumoniae infection by IL-23-dependent or independent mechanism.
authors.affiliation: Division of Host Defense, Medical Institute of Bioregulation, Kyushu University, Fukuoka.
authors.forename: Tesshin
authors.initials: T
authors.lastname: Murakami
authors.affiliation: Division of Host Defense, Medical Institute of Bioregulation, Kyushu University, Fukuoka.
authors.forename: Shinya
authors.initials: S
authors.lastname: Hatano
authors.affiliation: Division of Host Defense, Medical Institute of Bioregulation, Kyushu University, Fukuoka.
authors.forename: Hisakata
authors.initials: H
authors.lastname: Yamada
authors.affiliation: Center for Animal Disease Models, Research Institute for Biomedical Sciences, Tokyo University of Science, Noda, Japan.
authors.forename: Yoichiro
authors.initials: Y
authors.lastname: Iwakura
authors.affiliation: Division of Host Defense, Medical Institute of Bioregulation, Kyushu University, Fukuoka.
authors.forename: Yasunobu
authors.initials: Y
authors.lastname: Yoshikai
mesh_terms: D000818:Animals; D005260:Female; D020381:Interleukin-17 / Q000172:deficiency / Q000378:metabolism*; D053760:Interleukin-23 Subunit p19 / Q000378:metabolism; D007710:Klebsiella Infections / Q000276:immunology*; D007711:Klebsiella pneumoniae / Q000276:immunology*; D008810:Mice, Inbred C57BL; D018345:Mice, Knockout; D018410:Pneumonia, Bacterial / Q000276:immunology*; D013601:T-Lymphocytes / Q000276:immunology*
chemical_list: C098680:Il17a protein, mouse; C508841:Il23a protein, mouse; D020381:Interleukin-17; D053760:Interleukin-23 Subunit p19
keywords: CD69; IL-17A; IL-23; Klebsiella pneumoniae; Vγ1−Vγ4− γδ T cells; Vγ4 γδ T cells