期刊
INFECTION AND IMMUNITY
卷 81, 期 4, 页码 1090-1099出版社
AMER SOC MICROBIOLOGY
DOI: 10.1128/IAI.01199-12
关键词
-
资金
- NIAID, NIH [R01 AI-064522]
- DFG [SFB620, TP B2]
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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