title: Killer cell lectin-like receptor G1 deficiency significantly enhances survival after Mycobacterium tuberculosis infection.
abstract: The expression of T cell differentiation markers is known to increase during Mycobacterium tuberculosis infection, and yet the biological role of such markers remains unclear. We examined the requirement of the T cell differentiation marker killer cell lectin-like receptor G1 (KLRG1) during M. tuberculosis infection using mice deficient in KLRG1. KLRG1(-/-) mice had a significant survival extension after M. tuberculosis infection compared to wild-type controls, and maintained a significantly lower level of pulmonary M. tuberculosis throughout chronic infection. Improved control of M. tuberculosis infection was associated with an increased number of activated pulmonary CD4(+) T cells capable of secreting gamma interferon (IFN-γ). Our report is the first to show an in vivo impact of KLRG1 on disease control.
authors: Department of Microbial Infection and Immunity, The Ohio State University, Columbus, Ohio, USA.
authors: Joshua C
authors: JC
authors: Cyktor
authors: Bridget
authors: B
authors: Carruthers
authors: Paul
authors: P
authors: Stromberg
authors: Emilio
authors: E
authors: Flaño
authors: Hanspeter
authors: H
authors: Pircher
authors: Joanne
authors: J
authors: Turner
mesh_terms: D000818:Animals; D058491:Bacterial Load; D015496:CD4-Positive T-Lymphocytes / Q000276:immunology; D007371:Interferon-gamma / Q000378:metabolism; D037181:Lectins, C-Type; D008168:Lung / Q000382:microbiology / Q000473:pathology; D051379:Mice; D018345:Mice, Knockout; D009169:Mycobacterium tuberculosis / Q000276:immunology / Q000472:pathogenicity*; D011971:Receptors, Immunologic / Q000172:deficiency / Q000378:metabolism*; D016019:Survival Analysis; D014376:Tuberculosis / Q000276:immunology / Q000401:mortality / Q000473:pathology*
chemical_list: C451496:Klrg1 protein, mouse; D037181:Lectins, C-Type; D011971:Receptors, Immunologic; D007371:Interferon-gamma