A Batf3/Nlrp3/IL-18 Axis Promotes Natural Killer Cell IL-10 Production during Listeria monocytogenes Infection.
A Batf3/Nlrp3/IL-18 Axis Promotes Natural Killer Cell IL-10 Production during Listeria monocytogenes Infection.
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BATF3/Nlrp3/IL-18轴促进单核细胞增多性李斯特菌感染过程中自然杀伤细胞IL-10的产生。
DOI：
10.1016/j.celrep.2018.04.106
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发表时间：
2018-05-29
期刊：
影响因子：
8.8
通讯作者：
Lenz LL
中科院分区：
文献类型：
--
作者：
Clark SE;Schmidt RL;McDermott DS;Lenz LL
The bacterial pathogen Listeria monocytogenes (Lm) capitalizes on natural killer (NK) cell production of regulatory interleukin (IL)-10 to establish severe systemic infections. Here, we identify regulators of this IL-10 secretion. We show that IL-18 signals to NK cells license their ability to produce IL-10. IL-18 acts independent of IL-12 and STAT4, which co-stimulate IFNγ secretion. Dendritic cell (DC) expression of Nlrp3 is required for IL-18 release in response to the Lm p60 virulence protein. Therefore, mice lacking Nlrp3, Il18, or Il18R fail to accumulate serum IL-10 and are highly resistant to systemic Lm infection. We further show that cells expressing or dependent on Batf3 are required for IL-18-inducing IL-10 production observed in infected mice. These findings explain how Il18 and Batf3 promote susceptibility to bacterial infection and demonstrate the ability of Lm to exploit NLRP3 for the promotion of regulatory NK cell activity. Clark et al. show that a bacterial pathogen suppresses protective immunity through an inflammasome-dependent pathway. Stimulation of NLRP3-dependent interleukin (IL)-18 release licenses NK cells to produce the anti-inflammatory molecule IL-10. Batf3-dependent cells are vital for IL-18 release, which drives this regulatory natural killer cell activity.
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