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Publication : Killer cell lectin-like receptor G1 deficiency significantly enhances survival after Mycobacterium tuberculosis infection.

First Author  Cyktor JC Year  2013
Journal  Infect Immun Volume  81
Issue  4 Pages  1090-9
PubMed ID  23340310 Mgi Jnum  J:194060
Mgi Id  MGI:5470206 Doi  10.1128/IAI.01199-12
Citation  Cyktor JC, et al. (2013) Killer Cell Lectin-Like Receptor G1 Deficiency Significantly Enhances Survival after Mycobacterium tuberculosis Infection. Infect Immun 81(4):1090-9
abstractText  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-gamma). Our report is the first to show an in vivo impact of KLRG1 on disease control.
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