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| 1 | Human monoclonal antibodies block the binding of SARS-CoV-2 spike protein to angiotensin converting enzyme 2 receptor显示文摘According to the World Health Organization(WHO)newly updated situation report on March 18th,2020,the coronavirus disease 2019(COVID-19)pandemic has confirmed 191,127 cases and claimed 7807 deaths worldwide.1 The etiological agent of COVID-19 has been identified as a novel coronavirus,the severe acute respiratory syndrome coronavirus 2(SARS-CoV-2),belonging to Sarbecovirus subgenus(genus Betacoronavirus,family Coronaviridae)and showing 79.6 and 96.2%sequence identity in nucleotide to SARS-CoV and a bat coronavirus(BatCoV RaTG13),respectively.2–4 Like SARS-CoV infection,a substantial fraction of COVID-19 patients exhibits severe respiratory symptoms and has to be hospitalized in intensive care unit.5–8 Although the mortality rate of COVID-19 is significantly lower than that of SARS-CoV infection,SARS-CoV-2 shows much higher human-to-human transmission rate,rapidly leading to a global pandemic declared by WHO on March 11th,2020. | Xiangyu Chen Ren Li Zhiwei Pan Chunfang Qian Yang Yang Renrong You Jing Zhao Pinghuang Liu Leiqiong Gao Zhirong Li Qizhao Huang Lifan Xu Jianfang Tang Qin Tian Wei Yao Li Hu Xiaofeng Yan Xinyuan Zhou Yuzhang Wu Kai Deng Zheng Zhang Zhaohui Qian Yaokai Chen Lilin Ye | 2020 | Cellular & Molecular Immunology2020，17，6： | 17 |
| 2 | The histone methyltransferase EZH2 primes the early differentiation of follicular helper T cells during acute viral infection显示文摘Epigenetic modifications to histones dictate the differentiation of naïve CD4^(+) T cells into different subsets of effector T helper(TH)cells.The histone methyltransferase enhancer of zeste homolog 2(EZH2)has been implicated in the mechanism regulating the differentiation of TH1,TH2 and regulatory T(Treg)cells.However,whether and how EZH2 regulates follicular helper T(TFH)cell differentiation remain unknown.Using a mouse model of acute lymphocytic choriomeningitis virus(LCMV)infection,we observed abundant EZH2 expression and associated H3K27me3 modifications preferentially in the early committed virus-specific TFH cells compared to those in TH1 cells.Ablation of EZH2 in LCMV-specific CD4^(+) T cells leads to a selective impairment of early TFH cell fate commitment,but not late TFH differentiation or memory TFH maintenance.Mechanistically,EZH2 specifically stabilizes the chromatin accessibility of a cluster of genes that are important for TFH fate commitment,particularly B cell lymphoma 6(Bcl6),and thus directs TFH cell commitment.Therefore,we identified the chromatin-modifying enzyme EZH2 as a novel regulator of early TFH differentiation during acute viral infection. | Xiangyu Chen Guoshuai Cao Jialin Wu Xinxin Wang Zhiwei Pan Jianbao Gao Qin Tian Lifan Xu Zhirong Li Yaxing Hao Qizhao Huang Pengcheng Wang Minglu Xiao Luoyingzi Xie Shupei Tang Zhenyu Liu Li Hu Jianfang Tang Ran He Li Wang Xinyuan Zhou Yuzhang Wu Mengjie Chen Beicheng Sun Bo Zhu Jun Huang Lilin Ye | 2020 | Cellular & Molecular Immunology2020，17，3： | 4 |
| 3 | The dichotomous and incomplete adaptive immunity in COVID-19 patients with different disease severity显示文摘The adaptive immunity that protects patients from coronavirus disease 2019(COVID-19),caused by severe acute respiratory syndrome coronavirus 2(SARS-CoV-2),is not well characterized.In particular,the asymptomatic patients have been found to induce weak and transient SARS-CoV-2 antibody responses,but the underlying mechanisms remain unknown;meanwhile,the protective immunity that guide the recovery of these asymptomatic patients is elusive.Here,we characterized SARS-CoV-2-specific B-cell and T-cell responses in 10 asymptomatic patients and 64 patients with other disease severity(mild,n=10,moderate,n=32,severe,n=12)and found that asymptomatic or mild symptomatic patients failed to mount virus-specific germinal center(GC)B cell responses that result in robust and prolonged humoral immunity,assessed by GC response indicators including follicular helper T(TFH)cell and memory B cell responses as well as serum CXCL13 levels.Alternatively,these patients mounted potent virus-specific TH1 and CD8+T cell responses.In sharp contrast,patients of moderate or severe disease induced vigorous virus-specific GC B cell responses and associated TFH responses;however,the virus-specific TH1 and CD8+T cells were minimally induced in these patients.These results,therefore,uncovered the protective immunity in asymptomatic patients and also revealed the strikingly dichotomous and incomplete humoral and cellular immune responses in COVID-19 patients with different disease severity,providing important insights into rational design of effective COVID-19 vaccines. | Leiqiong Gao Jing Zhou Sen Yang Lisha Wang Xiangyu Chen Yang Yang Ren Li Zhiwei Pan Jing Zhao Zhirong Li Qizhao Huang Jianfang Tang Li Hu Pinghuang Liu Guozhong Zhang Yaokai Chen Lilin Ye | 2021 | Signal Transduction and Targeted Therapy2021，6，4： | 2 |
| 4 | CD49a^(+)CD49b^(+) NK cells induced by viral infection reflect an activated state of conventional NK cells显示文摘Natural killer(NK) cells are important innate effectors that play a pivotal role in the defense against tumors and infections and participate in regulating adaptive immunity. Recent studies have revealed phenotypic and functional heterogeneity of NK cells.Here, using murine models of acute and chronic lymphocytic choriomeningitis virus infection, we observed that a CD49a^(+)CD49b^(+) NK cell subset emerged in the liver and other tissues, and underwent vigorous expansion following viral infection,before progressively decreasing in cell number. These viral infection-induced CD49a^(+)CD49b^(+) NK cells displayed an activated and mature phenotype. Moreover, compared with liver-resident NK cells and conventional NK(cNK) cells, CD49a^(+)CD49b^(+) NK cells showed increased functional competence, as evidenced by higher amounts of IFN-γ production and stronger cytotoxic capabilities during viral infection. Generation of these CD49a^(+)CD49b^(+) NK cells was shown to be independent of the T-bet transcription factor. Adoptive transfer experiments revealed that c NK cells could convert into CD49a^(+)CD49b^(+) NK cells following viral infection. Collectively, these results suggest that viral infection-induced CD49a^(+)CD49b^(+) NK cells represent a transiently activated state of cNK cells. | Wenhan Li Jing Zhou Xianwei Wang Yuzhang Wu Lilin Ye Haiming Wei Rui Sun Zhigang Tian Hui Peng | 2020 | Science China(Life Sciences)2020，63，11： | 2 |
| 5 | Disease severity dictates SARS-CoV-2-specific neutralizing antibody responses in COVID-19显示文摘COVID-19 patients exhibit differential disease severity after SARS-CoV-2 infection.It is currently unknown as to the correlation between the magnitude of neutralizing antibody(NAb)responses and the disease severity in COVID-19 patients.In a cohort of 59 recovered patients with disease severity including severe,moderate,mild,and asymptomatic,we observed the positive correlation between serum neutralizing capacity and disease severity,in particular,the highest NAb capacity in sera from the patients with severe disease,while a lack of ability of asymptomatic patients to mount competent NAbs.Furthermore,the compositions of NAb subtypes were also different between recovered patients with severe symptoms and with mild-tomoderate symptoms.These results reveal the tremendous heterogeneity of SARS-CoV-2-specific NAb responses and their correlations to disease severity,highlighting the needs of future vaccination in COVID-19 patients recovered from asymptomatic or mild illness. | Xiangyu Chen Zhiwei Pan Shuai Yue Fei Yu Junsong Zhang Yang Yang Ren Li Bingfeng Liu Xiaofan Yang Leiqiong Gao Zhirong Li Yao Lin Qizhao Huang Lifan Xu Jianfang Tang Li Hu Jing Zhao Pinghuang Liu Guozhong Zhang Yaokai Chen Kai Deng Lilin Ye | 2020 | Signal Transduction and Targeted Therapy2020，5，1： | 1 |
| 6 | Distinct Memory CD4 + T Cells with Commitment to T Follicular Helper- and T Helper 1-Cell Lineages Are Generated after Acute Viral Infection显示文摘 | J. Scott Hale Ben Youngblood Donald R. Latner Ata Ur Rasheed Mohammed Lilin Ye Rama S. Akondy Tuoqi Wu Smita S. Iyer Rafi Ahmed | 2013 | Immunity2013，，4： | 1 |
| 7 | Efficient control of chronic LCMV infection by a CD4 T cell epitope-based heterologous prime-boost vaccination in a murine model显示文摘CD4^(+)T cells are essential for sustaining CD8^(+)T cell responses during a chronic infection.The adoptive transfer of virus-specific CD4^(+)T cells has been shown to efficiently rescue exhausted CD8^(+)T cells.However,the question of whether endogenous virus-specific CD4^(+)T cell responses can be enhanced by certain vaccination strategies and subsequently reinvigorate exhausted CD8^(+)T cells remains unexplored.In this study,we developed a CD4^(+)T cell epitope-based heterologous prime-boost immunization strategy and examined the efficacy of this strategy using a mouse model of chronic lymphocytic choriomeningitis virus(LCMV)infection.We primed chronically LCMV-infected mice with a Listeria monocytogenes vector that expressed the LCMV glycoprotein-specific I-Ab-restricted CD4^(+)T cell epitope GP61–80(LM-GP61)and subsequently boosted the primed mice with an influenza virus A(PR8 strain)vector that expressed the same CD4^(+)T cell epitope(IAV-GP61).This heterologous prime-boost vaccination strategy elicited strong anti-viral CD4^(+)T cell responses,which further improved both the quantity and quality of the virusspecific CD8^(+)T cells and led to better control of the viral loads.The combination of this strategy and the blockade of the programmed cell death-1(PD-1)inhibitory pathway further enhanced the anti-viral CD8^(+)T cell responses and viral clearance.Thus,a heterologous prime-boost immunization that selectively induces virus-specific CD4^(+)T cell responses in conjunction with blockade of the inhibitory pathway may represent a promising therapeutic approach to treating patients with chronic viral infections. | Ran He Xinxin Yang Cheng Liu Xiangyu Chen Lin Wang Minglu Xiao Jianqiang Ye Yuzhang Wu Lilin Ye | 2018 | Cellular & Molecular Immunology2018，15，9： | 1 |
| 8 | The m1A modification of tRNAs:a translational accelerator of T-cell activation显示文摘Upon antigen stimulation,naïve T cells exit the quiescent state and undergo rapid clonal expansion and differentiation[1].This cell fate transition requires accelerated protein synthesis,which is regulated at both the transcriptional and translational levels[2,3].Compared with well-documented transcriptional regulatory mechanisms,the translational regulation of T-cell activation has not been fully elucidated.A recent study by Liu et al. | Cheng Chen Lilin Ye | 2022 | Cellular & Molecular Immunology2022，19，12： | 1 |
| 9 | A potent human monoclonal antibody with pan-neutralizing activities directly dislocates S trimer of SARS-CoV-2 through binding both up and down forms of RBD显示文摘The severe acute respiratory syndrome coronavirus 2(SARS-CoV-2)has caused a global pandemic of novel coronavirus disease(COVID-19).The neutralizing monoclonal antibodies(mAbs)targeting the receptor-binding domain(RBD)of SARS-CoV-2 are among the most promising strategies to prevent and treat COVID-19.However,SARS-CoV-2 variants of concern(VOCs)profoundly reduced the efficacies of most of mAbs and vaccines approved for clinical use.Herein,we demonstrated mAb 35B5 efficiently neutralizes both wild-type(WT)SARS-CoV-2 and VOCs. | Xiaofei Wang Ao Hu Xiangyu Chen Yixin Zhang Fei Yu Shuai Yue Arong Li Junsong Zhang Zhiwei Pan Yang Yang Yao Lin Leiqiong Gao Jing Zhou Jing Zhao Fang Li Yaling Shi Feng Huang Xiaofan Yang Yi Peng Luoyang Tu Huan Zhang Huanying Zheng Jun He Hui Zhang Lifan Xu Qizhao Huang Yongqun Zhu Kai Deng Lilin Ye | 2022 | Signal Transduction and Targeted Therapy2022，7，5： | 1 |
| 10 | Aged hematopoietic stem cells entrap regulatory T cells to create a prosurvival microenvironment显示文摘Although DNA mutation drives stem cell aging,how mutation-accumulated stem cells obtain clonal advantage during aging remains poorly understood.Here,using a mouse model of irradiation-induced premature aging and middle-aged mice,we show that DNA mutation accumulation in hematopoietic stem cells(HSCs)during aging upregulates their surface expression of major histocompatibility complex class II(MHCII).MHCII upregulation increases the chance for recognition by bone marrow(BM)-resident regulatory T cells(Tregs),resulting in their clonal expansion and accumulation in the HSC niche.On the basis of the establishment of connexin 43(Cx43)-mediated gap junctions,BM Tregs transfer cyclic adenosine monophosphate(cAMP)to aged HSCs to diminish apoptotic priming and promote their survival via activation of protein kinase A(PKA)signaling.Importantly,targeting the HSC–Treg interaction or depleting Tregs effectively prevents the premature/physiological aging of HSCs.These findings show that aged HSCs use an active self-protective mechanism by entrapping local Tregs to construct a prosurvival niche and obtain a clonal advantage. | Weinian Liao Chaonan Liu Ke Yang Jun Chen Yiding Wu Shuzhen Zhang Kuan Yu Lisha Wang Li Ran Mo Chen Fang Chen Yang Xu Song Wang Fengchao Wang Qian Zhang Jinghong Zhao Lilin Ye Changhong Du Junping Wang | 2023 | Cellular & Molecular Immunology2023，20，10： | 0 |
| 11 | B7S1, a novel candidate for anti-tumor checkpoint blockade immunotherapy显示文摘Antigen-specific CD8+T cells play a critical role in eradicating transformed or virally infected cells. Upon recognition of cancerous or viral originated peptides, presented by antigen-presenting cells (APCs) in the form of peptide-MHC class I complex, CD8+T cells become activated, rapidly and extensively proliferate and differentiate into functionally competent effector cells. Following successfully and timely clearing transformed or virally infected cells, the majority of effector CD8+Tcells die of apoptosis. Concomitantly a small fraction (around 5%–10%) of effector CD8+T cells survive and progressively differentiate into long-lived and self-renewable memory CD8+T cells. When reencountering | Xiangyu Chen Lilin Ye | 2018 | Science China(Life Sciences)2018，61，9： | 0 |
| 12 | The lncRNA Snhgl-Vpsl3D vesicle trafficking system promotes memory CD8 T cell establishment via regulating the dual effects of IL-7 signaling显示文摘The efficient induction and long-term persistence of pathogen-specific memory CD8 T cells are pivotal to rapidly curb the reinfection.Recent studies indicated that long-noncoding RNAs expression is highly cell-and stage-specific during T cell development and differentiation,suggesting their potential roles in T cell programs.However,the key lncRNAs playing crucial roles in memory CD8 T cell establishment remain to be clarified.Through CD8 T cell subsets profiling of lncRNAs,this study found a key lncRNA-Snhgl with the conserved naivehl-effectorlo-memoryh,expression pattern in CD8 T cells of both mice and human,that can promote memory formation while impeding effector CD8 in acute viral infection.Further,Snhgl was found interacting with the conserved vesicle trafficking protein Vps13D to promote IL-7Ra membrane location specifically.With the deep mechanism probing,the results show Snhgl-Vps13D regulated IL-7 signaling with its dual effects in memory CD8 generation,which not just because of the sustaining role of STAT5-BCL-2 axis for memory survival,but more through the STAT3-TCF1-Blimp1 axis for transcriptional launch program of memory differentiation.Moreover,we performed further study with finding a similar high-low-high expression pattern of human SNHG1A/PS13D/IL7R/TCF7 in CD8 T cell subsets from PBMC samples of the convalescent COVID-19 patients.The central role of Snhgl-Vps13D-IL-7R-TCF1 axis in memory CD8 establishment makes it a potential target for improving the vaccination effects to control the ongoing pandemic. | Yanyan Zhang Baohua Li Qiang Bai Pengcheng Wang Gang Wei Zhirong Li Li Hu Qin Tian Jing Zhou Qizhao Huang Zhiming Wang Shuai Yue Jialin Wu Liuqing Yang Xinyuan Zhou Lubin Jiang Ting Ni Lilin Ye Yuzhang Wu | 2021 | Signal Transduction and Targeted Therapy2021，6，4： | 0 |
| 13 | Tumor-specific memory CD8^(+)T cells are strictly resident in draining lymph nodes during tumorigenesis显示文摘The functional exhaustion of CD8^(+)T cells represents a fundamental hallmark of chronic viral infection and cancer and,in both scenarios,is driven by prolonged exposure to persistent cognate antigens in the context of an immunoinhibitory microenvironment.Exhausted CD8^(+)T cells upregulate the expression of a wide diversity of coinhibitory immunoreceptors(also referred to as immune checkpoint receptors),such as PD-1,Tim-3,LAG-3,and TIGIT.Concomitantly,exhausted CD8^(+)T cells lose their potential to differentiate into functional memory cells and are characterized by hierarchical loss of effector function,leading to compromised tumor control and viral eradication[1,2]. | Qiao Liu Ling Ran Zhengliang Yue Xingxing Su Lisha Wang Shuqiong Wen Shun Lei Xiaofan Yang Yan Zhang Jianjun Hu Jianfang Tang Zhirong Li Li Hu Bo Zhu Lifan Xu Lilin Ye Qizhao Huang | 2023 | Cellular & Molecular Immunology2023，20，4： | 0 |
| 14 | Author Correction:Tumor-specific memory CD8^(+)T cells are strictly resident in draining lymph nodes during tumorigenesis显示文摘 | Qiao Liu Ling Ran Zhengliang Yue Xingxing Su Lisha Wang Shuqiong Wen Shun Lei Xiaofan Yang Yan Zhang Jianjun Hu Jianfang Tang Zhirong Li Li Hu Bo Zhu Lifan Xu Lilin Ye Qizhao Huang | 2023 | Cellular & Molecular Immunology2023，20，7： | 0 |
| 15 | DAPK1(death associated protein kinase 1)mediates mTORC1 activation and antiviral activities in CD8^(+)T cells显示文摘Mechanistic target of rapamycin complex 1(mTORCt)regulates CD8^(+)T-cell differentiation and function.Despite the links between PI3K-AKT and mTORCI activation in CD8^(+)T cells,the molecular mechanism underlying mTORCI activation remains undear.Here,we show that both the kinase activity and the death domain of DAPK1 are required for maximal mTOR activation and CD8^(+)T-cell function.We found that TCR-induced activation of calcineurin activates DAPK1,which subsequently interacts with TSC2 via its death domain and phosphorylates TSC2 to mediate mTORCI activation.Furthermore,both the kinase domain and death domain of DAPK1 are required for CD8^(+)T-cell antiviral responses in an LCMV infection model.Together,our data reveal a novel mechanism of mTORCI activation that mediates optimal CD8^(+)T-cell function and antiviral activity. | Zhengping Wei Pingfei Li Ran He Huicheng Liu Na Liu Yu Xia Guoyu Bi Qiuyang Du Minghui Xia Lei Pei Jing Wang Guihua Wang Zhao-Hui Tang Xiang Cheng Huabin Li Zhuoya Li Lilin Ye Arian Laurence Youming Lu Xiang-Ping Yang | 2021 | Cellular & Molecular Immunology2021，18，1： | 0 |
| 16 | A novel linear and broadly neutralizing peptide in the SARS-CoV-2 S2 protein for universal vaccine development显示文摘As humans continue to develop COVID-19 widely,numerous novel variants of SARS-CoV-2 have emerged[1,2].These variants,which may possess enhanced transmissibility and often result in breakthrough infections in the vaccinated population,pose great challenges to the current vaccine strategies targeting the immunodominance of the receptor-binding domain(RBD)of the spike(S)protein[2]. | Tuofan Li Qiuqi Kan Jinying Ge Zhimin Wan Mengqi Yuan Yao Huang Quan Xie Yi Yang Hongxia Shao Xiangdong Li Lilin Ye Aijian Qin Zhigao Bu Pinghuang Liu Jianqiang Ye | 2021 | Cellular & Molecular Immunology2021，18，11： | 0 |
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