title: NK cells respond to pulmonary infection with Mycobacterium tuberculosis, but play a minimal role in protection.
abstract: Both innate and adaptive immune systems contribute to host defense against infection with Mycobacterium tuberculosis. NK cells have been associated with early resistance against intracellular pathogens and are known to be potent producers of the cytokine IFN-gamma. In C57BL/6 mice infected by aerosol exposure with M. tuberculosis, NK cells increased in the lungs over the first 21 days of infection. Expansion of the NK cell subset was associated with increased expression of activation and maturation markers. In addition, NK cells isolated from the infected lungs were capable of producing IFN-gamma and became positive for perforin. In vivo depletion of NK cells using a lytic Ab had no influence on bacterial load within the lungs. These findings indicate that NK cells can become activated during the early response to pulmonary tuberculosis in the mouse model and are a source of IFN-gamma, but their removal does not substantially alter the expression of host resistance.
authors.affiliation: Department of Microbiology, Immunology, and Pathology, Colorado State University, Fort Collins, CO 80523, USA. ana.kipnis@colostate.edu
authors.forename: Ana Paula
authors.initials: AP
authors.lastname: Junqueira-Kipnis
authors.forename: Andre
authors.initials: A
authors.lastname: Kipnis
authors.forename: Amanda
authors.initials: A
authors.lastname: Jamieson
authors.forename: Mercedes Gonzalez
authors.initials: MG
authors.lastname: Juarrero
authors.forename: Andreas
authors.initials: A
authors.lastname: Diefenbach
authors.forename: David H
authors.initials: DH
authors.lastname: Raulet
authors.forename: Joanne
authors.initials: J
authors.lastname: Turner
authors.forename: Ian M
authors.initials: IM
authors.lastname: Orme
mesh_terms: D000280:Administration, Inhalation; D000336:Aerosols; D000818:Animals; D000941:Antigens / Q000096:biosynthesis; D015703:Antigens, CD / Q000096:biosynthesis; D000945:Antigens, Differentiation, T-Lymphocyte / Q000096:biosynthesis; D000954:Antigens, Surface; D039481:CD11b Antigen / Q000096:biosynthesis; D002465:Cell Movement / Q000276:immunology; D002478:Cells, Cultured; D003602:Cytotoxicity, Immunologic / Q000276:immunology*; D005260:Female; D016130:Immunophenotyping; D007371:Interferon-gamma / Q000096:biosynthesis; D007694:Killer Cells, Natural / Q000276:immunology* / Q000378:metabolism / Q000382:microbiology* / Q000473:pathology; D037181:Lectins, C-Type; D008168:Lung / Q000276:immunology / Q000382:microbiology / Q000473:pathology; D008212:Lymphocyte Depletion; D008562:Membrane Glycoproteins / Q000096:biosynthesis; D051379:Mice; D008810:Mice, Inbred C57BL; D009169:Mycobacterium tuberculosis / Q000276:immunology*; D055651:NK Cell Lectin-Like Receptor Subfamily B; D009330:Nebulizers and Vaporizers; D054353:Perforin; D052899:Pore Forming Cytotoxic Proteins; D014176:Protein Biosynthesis; D011506:Proteins; D011971:Receptors, Immunologic / Q000096:biosynthesis; D055607:Receptors, Natural Killer Cell; D000071176:Signaling Lymphocytic Activation Molecule Family; D014397:Tuberculosis, Pulmonary / Q000276:immunology* / Q000382:microbiology* / Q000517:prevention & control; D000099192:CD69 Antigens
chemical_list: D000336:Aerosols; D000941:Antigens; D015703:Antigens, CD; D000945:Antigens, Differentiation, T-Lymphocyte; D000954:Antigens, Surface; D039481:CD11b Antigen; D007371:Interferon-gamma; D037181:Lectins, C-Type; D008562:Membrane Glycoproteins; D055651:NK Cell Lectin-Like Receptor Subfamily B; D054353:Perforin; D052899:Pore Forming Cytotoxic Proteins; D011506:Proteins; D011971:Receptors, Immunologic; D055607:Receptors, Natural Killer Cell; D000071176:Signaling Lymphocytic Activation Molecule Family; D000099192:CD69 Antigens; C490007:Cd244a protein, mouse