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| 1 | Innate recognition of microbial-derived signals in immunity and inflammation显示文摘Microbes generate a vast array of different types of conserved structural components called pathogen-associated molecular patterns(PAMPs),which canbe recognized by cells of the innate immune system.This recognition of 'nonself' signatures occurs through host pattern recognition receptors(PRRs),suggesting that microbial-derived signals are good targets for innate immunity to discriminate between self- and nonself.Such PAMP-PRR interactions trigger multiple but distinct downstream signaling cascades,subsequently leading to production of proinflammatory cytokines and interferons that tailor immune responses to particular microbes.Aberrant PRR signals have been associated with various inflammatory diseases and fine regulation of PRR signaling is essential for avoiding excessive inflammatory immune responses and maintaining immune homeostasis.In this review we summarize the ligands and signal transduction pathways of PRRs and highlight recent progress of the mechanisms involved in microbe-specific innate immune recognition during immune responses and inflammation,which may provide new targets for therapeutic intervention to the inflammatory disorders. | Yue Zhang Chunli Liang | 2016 | Science China(Life Sciences)2016，59，12： | 14 |
| 2 | 单核/巨噬细胞发生受训后免疫的机制研究进展显示文摘只有适应性免疫系统才具有记忆性的传统观点目前正逐渐受到挑战。在缺乏适应性免疫的生物体(植物、无脊椎动物)以及脊椎动物体内,均发现了固有免疫系统(自然杀伤细胞、单核/巨噬细胞等)在再次接触相同或无关病原体刺激时表现出增强或减弱的免疫反应,这一现象被称为受训后免疫(TI)或固有免疫记忆。经典的适应性免疫记忆具有特异性、抗原依赖性、由基因重排介导等特点,而TI则被认为是非特异性的、抗原无关的、由表观遗传学及代谢重编程介导的,因此TI是机体免疫记忆的一种新补充。研究证实TI是一把双刃剑,在维持健康和促进疾病中发挥重要作用;阐明TI的调控机制,将为感染性疾病、免疫缺陷病及炎症疾病等疾病的发病机理研究以及新型疫苗的研发提供新颖视角。本文对TI的发现、特点、发生机制等方面进行综述,重点阐述表观遗传学及代谢重编程在单核巨噬细胞发生TI中的作用及最新的机制研究进展。 | 张欣 钱心玉 杨晓莹(指导) 潘伟 | 2019 | 中国免疫学杂志2019，35，21： | 5 |
| 3 | Neutrophil programming dynamics and its disease relevance显示文摘Neutrophils are traditionally considered as first responders to infection and provide antimicrobial host defense. However, recent advances indicate that neutrophils are also critically involved in the modulation of host immune environments by dynamically adopting distinct functional states. Functionally diverse neutrophil subsets are increasingly recognized as critical components mediating host pathophysiology. Despite its emerging significance, molecular mechanisms as well as functional relevance of dynamically programmed neutrophils remain to be better defined. The increasing complexity of neutrophil functions may require integrative studies that address programming dynamics of neutrophils and their pathophysiological relevance. This review aims to provide an update on the emerging topics of neutrophil programming dynamics as well as their functional relevance in diseases. | Taojing Ran Shuo Geng Liwu Li | 2017 | Science China(Life Sciences)2017，60，11： | 3 |
| 4 | Endothelial Notch activation promotes neutrophil transmigration via downregulating endomucin to aggravate hepatic ischemia/reperfusion injury显示文摘Inflammatory leukocytes infiltration is orchestrated by mechanisms involving chemokines,selectins,addressins and other adhesion molecules derived from endothelial cells(ECs),but how they respond to inflammatory cues and coordinate leukocyte transmigration remain elusive.In this study,using hepatic ischemia/reperfusion injury(HIRI)as a model,we identified that endothelial Notch activation was rapidly and dynamically induced in liver sinusoidal endothelial cells(LSECs)in acute inflammation.In mice with EC-specific Notch activation(NICeCA),HIRI induced exacerbated liver damage.Consistently,endothelial Notch activation enhanced neutrophil infiltration and tumor necrosis factor(TNF)-αexpression in HIRI.Transcriptome analysis and further qRT-PCR as well as immunofluorescence indicated that endomucin(EMCN),a negative regulator of leukocyte adhesion,was downregulated in LSECs from NICeCA mice.EMCN was downregulated during HIRI in wild-type mice and in vitro cultured ECs insulted by hypoxia/re-oxygenation injury.Notch activation in ECs led to increased neutrophil adhesion and transendothelial migration,which was abrogated by EMCN overexpression in vitro.In mice deficient of RBPj,the integrative transcription factor of canonical Notch signaling,although overwhelming sinusoidal malformation aggravated HIRI,the expression of EMCN was upregulated;and pharmaceutical Notch blockade in vitro also upregulated EMCN and inhibited transendothelial migration of neutrophils.The Notch activation-exaggerated HIRI was compromised by blocking LFA-1,which mediated leukocyte adherence by associating with EMCN.Therefore,endothelial Notch signaling controls neutrophil transmigration via EMCN to modulate acute inflammation in HIRI. | Peiran Zhang Kangyi Yue Xinli Liu Xianchun Yan Ziyan Yang Juanli Duan Congcong Xia Xinyuan Xu Mei Zhang Liang Liang Lin Wang Hua Han | 2020 | Science China(Life Sciences)2020，63，3： | 1 |
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