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文章简介NK细胞数量和功能异常与肿瘤和持续性病毒感染的发生密切相关。目前对于在NK细胞激活过程中,表观遗传机制如何参与调控细胞因子刺激的信号通路仍知之甚少。研究证实,组蛋白去甲基化酶Kdm5a对于NK细胞的发育和成熟并不是必须的,但Kdm5a缺陷会破坏NK细胞的激活,降低IFN-γ的生成。结合LM感染
Article introduction NK cell number and dysfunction and tumor and persistent virus infection are closely related. At present, little is known about how epigenetic mechanisms are involved in the regulation of cytokine-stimulated signaling during NK cell activation. The study confirmed that histone demethylase Kdm5a for NK cell development and maturation is not necessary, but Kdm5a defects will destroy the activation of NK cells and reduce IFN-γ production. Combine LM infection