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.

journal_name

Infect Immun

journal_title

Infection and immunity

authors

Cyktor JC,Carruthers B,Stromberg P,Flaño E,Pircher H,Turner J

doi

10.1128/IAI.01199-12

subject

Has Abstract

pub_date

2013-04-01 00:00:00

pages

1090-9

issue

4

eissn

0019-9567

issn

1098-5522

pii

IAI.01199-12

journal_volume

81

pub_type

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