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Front Immunol. 2017 Feb 13;8:123. doi: 10.3389/fimmu.2017.00123. eCollection 2017.

FHL2 Regulates Natural Killer Cell Development and Activation during Streptococcus pneumoniae Infection.

Author information

1
INSERM, Centre d'Etude des Pathologies Respiratoires (CEPR), UMR 1100, Tours, France; Université François Rabelais, Tours, France.
2
INSERM, Centre d'Etude des Pathologies Respiratoires (CEPR), UMR 1100, Tours, France; Université François Rabelais, Tours, France; Service de Réanimation Polyvalente, Centre Hospitalier Régional Universitaire, Tours, France.
3
Centre d'Immunologie de Marseille-Luminy, Aix Marseille Université, INSERM, CNRS , Marseille , France.
4
Centre d'Immunologie de Marseille-Luminy, Aix Marseille Université, INSERM, CNRS, Marseille, France; Hôpital de la Timone, Assistance Publique-Hôpitaux de Marseille, Marseille, France.
5
ISP, INRA, Université Tours , Nouzilly , France.
6
Hépacivirus et immunité innée, Institut Pasteur , Paris , France.

Abstract

Recent in silico studies suggested that the transcription cofactor LIM-only protein FHL2 is a major transcriptional regulator of mouse natural killer (NK) cells. However, the expression and role of FHL2 in NK cell biology are unknown. Here, we confirm that FHL2 is expressed in both mouse and human NK cells. Using FHL2-/- mice, we found that FHL2 controls NK cell development in the bone marrow and maturation in peripheral organs. To evaluate the importance of FHL2 in NK cell activation, FHL2-/- mice were infected with Streptococcus pneumoniae. FHL2-/- mice are highly susceptible to this infection. The activation of lung NK cells is altered in FHL2-/- mice, leading to decreased IFNγ production and a loss of control of bacterial burden. Collectively, our data reveal that FHL2 is a new transcription cofactor implicated in NK cell development and activation during pulmonary bacterial infection.

KEYWORDS:

FHL2; NK cell; maturation; mouse models; pneumococcal infections; transcriptional factor

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