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KDM2B promotes IL-6 production and inflammatory responses through Brg1-mediated chromatin remodeling

Cellular & Molecular Immunology 2020年第8期17卷 834-842页

作者： Qingqing Zhou Yunkai zhang Bo Wang Wenhui Zhou Yong Bi Wanwan Huai Xi Chen Yihan Chen Zhongmin Liu Xingguang Liu zhenzhen zhan Institute of Heart Failure Shanghai East HospitalTongji University School of Medicine200120ShanghaiChina National Key Laboratory of Medical Immunology&Institute of Immunology Second Military Medical University200433ShanghaiChina Shanghai Fourth People’s Hospital Tongji University School of Medicine200081ShanghaiChina Institute of Immunology Zhejiang University School of Medicine310058HangzhouChina Key Laboratory of Arrhythmias of the Ministry of Education of China Shanghai East HospitalTongji University School of Medicine200120ShanghaiChina

IL-6 plays important and pleiotropic roles in infection and inflammatory diseases,and its production needs to be tightly regulated.However,the epigenetic mechanism underlying Il6 gene transcription remains to be fully elucidated.Here,we report that lysine-specific demethylase 2b(KDM2B),which demethylates H3K4me3 and H3K36me2,is required in macrophages and dendritic cells for the induction of IL-6 but not TNF-α,IL-1,and IFN-β.Compared to wild-type mice,KDM2B-deficient mice were more resistant to endotoxin shock and colitis,with a less severe inflammatory pathogenesis phenotype and decreased IL-6 production in sera.KDM2B selectively bound the Il6 promoter but did not alter histone demethylation;instead,KDM2B interacted with Brahma-related gene 1(Brg1),the core ATPase subunit of SWI/SNF chromatin remodeling complexes,to facilitate chromatin accessibility of the Il6 promoter.Furthermore,KDM2B directly recruited RNA Polymerase II to further initiate and promote Il6 transcription.Thus,our finding identifies a novel nonclassical function of KDM2B in gene-specific transcription initiation and enhancement of Il6 independent of its demethylase activity and adds new insight into the specific epigenetic modification mechanism of inflammatory immune responses.

关键词： KDM2B IL-6 Brg1 Chromatin remodeling Inflammation

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Kdm2b epigenetically promotes innate IL-6 production through Brg1-mediated chromatin remodeling

Kdm2b epigenetically promotes innate IL-6 production through...

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第十三届全国免疫学学术大会

作者： zhenzhen zhan Qingqing Zhou Yunkai zhang Bo Wang Institute of Heart Failure Shanghai East HospitalTongji University School of Medicine National Key Laboratory of Medical Immunology & Institute of Immunology Second Military Medical University

Interleukin-6(IL-6) plays important and pleiotropic roles in infection and inflammatory diseases, and its production needs to be tightly regulated. However, the epigenetic mechanism underlying Il6 gene transcription remains to be fully elucidated. Here, we reported that deficiency of lysine-specific demethylase 2 b(Kdm2 b), a demethylase of H3 K36 me2 and H3 K4 me3, preferentially inhibited innate IL-6 production triggered by Toll-like receptors(TLRs) in macrophages and dendritic cells, but not the production of TNF-α and IFN-β. Kdm2 b-deficient mice were more resistant to LPS-or poly(I:C)-triggered endotoxin shock and dextran-sulfate-sodium(DSS)-induced colitis with a decreased IL-6 production and less severe inflammatory pathogenesis phenotype. Kdm2 b selectively bound the Il6 promoter, but did not alter the histone demethylation;instead, Kdm2 b interacted with Brg1, the core ATPase subunit of SWI/SNF chromatin remodeling complexes, to facilitate the chromatin accessibility of Il6 promoter. Furthermore, Kdm2 b directly recruited RNA Polymerase II(Pol II)(RNAP II) to Il6 promoter. In all, Kdm2 b contributed to increased Il6 transcription upon innate stimuli. Our finding elucidated a crucial role of Kdm2 b in the gene-specific transcription initiation and enhancement of Il6 independent of its demethylase activity, and added a mechanic insight into the epigenetic modification of inflammatory immune responses.

关键词： KDM2B epigenetic regulation IL-6 macrophages inflammation

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Phosphatase PP4 negatively regulates antiviral innate immune response by dephosphorylating TBK1 in macrophages

Phosphatase PP4 negatively regulates antiviral innate immune...

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第九届全国免疫学学术大会

作者： zhenzhen zhan Xingguang Liu Huimin Fan Zhongmin Liu Research Center for Translational Medicine & Institute of heart failure

Effective recognition of viral infections and subsequent production of type I interferon are essential for the host antiviral innate immune responses.Type I IFN expression is tightly regulated by multiple intracellular regulators to prevent the development of immunopathological disorders and the harm to host.The phosphorylation and activation of serine/threonine kinase TBK1 plays an essential role in mediating type I interferon production.However,how the activated TBK1 is negatively regulated by its phosphatases)remains poorly understood.In this study,we report that PP4 expression was upregulated in Sendai virus(SeV)-and vesicular stomatitis virus(VSV)-infected macrophages.PP4 inhibited type I interferon production in macrophages triggered by SeV and VSV,thus enhanced RNA virus replication.Overexpression of a phosphatase-dead PP4 mutant(PP4-RL)abolished the inhibitory effects on type I interferon production.Accordingly,PP4 knockdown increased RNA virus-triggered type I IFN production and inhibited RNA virus replication.Moreover,PP4 directly interacted with TBK1 upon virus infection then dephosphorylated TBK1 at Serl72 and inhibited TBK1 activation,and subsequently suppressed IRF3 activation,resulting in suppression of virus-triggered innate immune response.Thus,PP4 functions as a feedback-negative regulator of RNA virus-triggered innate immune responses by function as a TBK1 phosphatase and suppress its activation.

关键词： Innate immunity PP4 TBK1 Type I IFN

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Allelic reprogramming of chromatin states in human early embryos

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National Science Review 2024年第3期11卷 58-71页

作者： Shenli Yuan Lei Gao Wenrong Tao Jianhong zhan Gang Lu Jingye zhang Chuanxin zhang Lizhi Yi Zhenbo Liu zhenzhen Hou Min Dai Han Zhao Zi-Jiang Chen Jiang Liu Keliang Wu Center for Reproductive Medicine Shandong University CAS Key Laboratory of Genome Sciences and Information Collaborative Innovation Center of Genetics and Development Beijing Institute of Genomicsand China National Center for BioinformationChinese Academy of Sciences University of Chinese Academy of Sciences CUHK-SDU Joint Laboratory on Reproductive Genetics School of Biomedical Sciences the Chinese University of Hong Kong Key Laboratory of Reproductive Endocrinology of the Ministry of Education Shandong University Center for Reproductive Medicine Ren Ji Hospital School of Medicine Shanghai Jiao Tong University CAS Center for Excellence in Animal Evolution and Genetics Chinese Academy of Sciences

The reprogramming of parental epigenomes in human early embryos remains elusive. To what extent the characteristics of parental epigenomes are conserved between humans and mice is currently unknown. Here,we mapped parental haploid epigenomes using human parthenogenetic and androgenetic embryos. Human embryos have a larger portion of genome with parentally specific epigenetic states than mouse embryos.The allelic patterns of epigenetic states for orthologous regions are not conserved between humans and mice. Nevertheless, it is conserved that maternal DNA methylation and paternal H3K27me3 are associated with the repression of two alleles in humans and mice. In addition, for DNA-methylation-dependent imprinting, we report 19 novel imprinted genes and their associated germline differentially methylated regions. Unlike in mice, H3K27me3-dependent imprinting is not observed in human early embryos.Collectively, allele-specific epigenomic reprogramming is different in humans and mice.

关键词： human embryo epigenetics reprogramming DNA methylation H3K27me3 chromatin accessibility

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A core-shell structured COYID-19 mRNA vaccine with favorable biodistribution pattern and promising immunity

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Signal Transduction and Targeted Therapy 2021年第6期6卷 1920-1929页

作者： Ren Yang Yao Deng Baoying Huang Lei Huang Ang Lin Yuhua Li Wenling Wang Jingjing Liu Shuaiyao Lu zhenzhen zhan Yufei Wang Ruhan A Wen Wang Peihua Niu Li Zhao Shiqiang Li Xiaopin Ma Luyao zhang Yujian zhang Weiguo Yao Xingjie Liang Jincun Zhao Zhongmin Liu Xiaozhong Peng Hangwen Li Wenjie Tan NHC Key Laboratory of Biosafety National Institute for Viral Disease Control and PreventionChinese Center for Disease Control and PreventionBeijingChina Stemirna Therapeutics ShanghaiChina National Institute for Food and Drug Control BeijingChina National Kunming High-level Primate Research Center Institute of Medical BiologyChinese Academy of Medical Sciences and Peking Union Medical CollegeYunnanChina Shanghai East Hospital Tongji UniversityShanghaiChina CAS Center for Excellence in Nanoscience CAS Key Laboratory for Biomedical Effects of Nanomaterials and NanosafetyChinese Academy of Sciences and National Center for Nanoscience and Technology of ChinaBeijingChina University of Chinese Academy of Sciences BeijingChina State Key Laboratory of Respiratory Disease National Clinical Research Center for Respiratory DiseaseGuangzhou Institute of Respiratory HealthThe First Affiliated Hospital of Guangzhou Medical UniversityGuangzhouGuangdongChina Center for Biosafety Mega-Science Chinese Academy of SciencesWuhanHubeiChina

Although inoculation of COVID-19 vaccines has rolled out globally,there is still a critical need for safe and effective vaccines to ensure fair and equitable supply for all countries.Here,we report on the development of a highly efficacious mRNA vaccine,SW0123 that is composed of sequence-modified mRNA encoding the full-length SARS-CoV-2 Spike protein packaged in core-shell structured lipopolyplex(LPP)nanoparticles.SWOT 23 is easy to produce using a large-scale microfluidics-based apparatus.The unique core-shell structured nanoparticle facilitates vaccine uptake and demonstrates a high colloidal stability,and a desirable biodistribution pattern with low liver targeting effect upon intramuscular administration.Extensive evaluations in mice and nonhuman primates revealed strong immunogenicity of SW0123,represented by induction of Th1-polarized T cell responses and high levels of antibodies that were capable of neutralizing not only the wild-type SARS-CoV-2,but also a panel of variants including D614G and N501Y variants.In addition,SW0123 conferred effective protection in both mice and non-human primates upon SARS-CoV-2 challenge.Taken together,SW0123 is a promising vaccine candidate that holds prospects for further evaluation in humans.

关键词： vaccine pattern immunity

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Zinc finger protein DPZF promotes TLR-triggered innate immunity by repressing IkBa gene transcription in macrophages

Zinc finger protein DPZF promotes TLR-triggered innate immun...

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第九届全国免疫学学术大会

作者： Xingguang Liu Peng zhang Qian zhang zhenzhen zhan Jun Meng Nan Li Xuetao Cao National Key Laboratory of Medical Immunology & Institute of Immunology Second Military Medical University

Background:The ability of the innate immune system to recognize and eliminate invading microbial pathogens has been largely attributed to Toll-like receptors(TLRs)and TLR-triggered immune response.Although many factors mediate the transduction of TLR signals,the molecular mechanisms involved in the full activation of TLR-triggered innate immunity remain to be fully elucidated.Dendritic cell-derived BTB/POZ zinc finger(DPZF)also named as HOF and ZNF288,belongs to BTB/POZ(broad complex tramtrack bric-a-brac/poxvirus and zinc finger)zinc finger family.DPZF was found to participate in neurogenesis and function as a key transcription repressor of alpha-fetoprotein gene in liver.However,the roles of DPZF in immune system remain unknown.Method:Myeloid cell-specific DPZF knockout mice were generated by repeated mating of DPZFmice with LysMcre mice.The endotoxin shock mouse model was established by intraperitoneal(i.p.)injection of 15 mg/kg LPS.For bacterial infection,mice were given intraperitoneal injection of 1 x 10’E.coli or intravenous injection of 1×10L.monocytogenes.Chromatin was immunoprecipitated according to the toinstructions instructions of the EZ ChIP kit.Results:Here we generated myeloid cell-specific DPZF knockout mice by the LysM-Cre/loxP approach and found these mice were resistant to endotoxin shock and Escherichia co//’-caused sepsis.DPZF deficiency attenuated the TLRtriggered production of proinflammatory’cytokines and type I interferon in macrophages,which attributed to the higher abundance of IkBa and impaired activity of the transcription factor NF-kB.Futhermore,chromatin immunoprecipitation(ChIP)-sequence assay showed that DPZF specifically bound to IkBa gene promoter(+1 to+60 region)after TLR activation.We found that DPZF was a transcriptional repressor capable of specifically inhibiting IkBa promoter-driven transcriptional activity.Therefore,DPZF functions a key regulator governing IkBa gene transcription,inhibits IkBa protein expression and enhances NF-kB activation,which leading to enhanced TLR

关键词： DPZF Toll-like receptor IkBa Transcription repression Innate immunity

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Zinc finger protein ZBTB20 promotes TLRtriggered innate immune responses by repressing IκBα gene transcription

Zinc finger protein ZBTB20 promotes TLRtriggered innate immu...

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第八届全国免疫学学术大会

作者： Xingguang Liu Peng zhang Yanmei Han Qian zhang Jun Meng zhenzhen zhan Yingke Li Nan Li Weiping zhang Xuetao Cao National Key Laboratory of Medical Immunology & Institute of Immunology Second Military Medical University

The ability of the innate immune system to recognize and eliminate invading microbial pathogens has been largely attributed to Toll-like receptors(TLRs)and TLR-triggered immune response.Although many factors mediate the transduction of TLR signals,the molecular mechanisms involved in the full activation of TLRtriggered innate immunity remain to be fully elucidated.ZBTB20,also named DPZF,HOF,and ZNF288,belongs to BTB/POZ(broad complex tramtrack bric-a-brac/poxvirus and zinc finger)zinc finger family.

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炎症反应在心肌再生中的作用

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中国比较医学杂志 2020年第11期30卷 128-132页

作者：谈勇占贞贞同济大学附属东方医院上海200120

目前因为心血管疾病而死的人数占所有患病死亡人数的30%以上。在这些患者中,急性心肌梗死通常是第一表现,可能进一步发展为心力衰竭。而人的心脏表现出低再生能力,导致了心肌细胞的不可逆损失和持久性的组织瘢痕,这必然带来严重的病理... 详细信息

目前因为心血管疾病而死的人数占所有患病死亡人数的30%以上。在这些患者中,急性心肌梗死通常是第一表现,可能进一步发展为心力衰竭。而人的心脏表现出低再生能力,导致了心肌细胞的不可逆损失和持久性的组织瘢痕,这必然带来严重的病理后遗症,我们迫切需要新的治疗方法,实现心肌再生。该文主要概述心肌再生这十几年的研究情况及炎症反应在其中的作用,为实现人体心肌再生提供方向。

关键词：心肌再生炎症反应巨噬细胞

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心肌纤维化的表观遗传调控研究进展

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中国比较医学杂志 2019年第3期29卷 92-97页

作者：汪波占贞贞曾麒燕广西医科大学生物化学与分子生物学教研室南宁530021 同济大学附属东方医院心力衰竭研究所上海200120

心力衰竭是慢性心血管疾病终末期死亡的主要因素之一,心肌不良重构在心力衰竭的发生中起到关键性作用,而心肌纤维化是心肌不良重构的一个重要表现。越来越多的研究表明,表观遗传调控机制在心肌纤维化的发生及发展过程中发挥重要的作用... 详细信息

心力衰竭是慢性心血管疾病终末期死亡的主要因素之一,心肌不良重构在心力衰竭的发生中起到关键性作用,而心肌纤维化是心肌不良重构的一个重要表现。越来越多的研究表明,表观遗传调控机制在心肌纤维化的发生及发展过程中发挥重要的作用。本文主要综述了DNA甲基化修饰、组蛋白修饰以及microRNA等表观遗传机制调控心肌纤维化发生发展的研究进展。

关键词：心肌纤维化表观遗传调控 DNA修饰组蛋白修饰 microRNA

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Analyzing the Effect of the Intra-Pixel Position of Small PSFs for Optimizing the PL of Optical Subpixel Localization

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Engineering 2023年第8期27卷 140-149页

作者： Haiyang zhan Fei Xing Jingyu Bao Ting Sun zhenzhen Chen Zheng You Li Yuan Department of Precision Instrument Tsinghua UniversityBeijing 100084China State Key Laboratory of Precision Measurement Technology and Instruments Tsinghua UniversityBeijing 100084China Beijing Advanced Innovation Center for Integrated Circuits Tsinghua UniversityBeijing 100084China Joint International Research Laboratory of Advanced Photonics and Electronics Beijing Information Science and Technology UniversityBeijing 100192China Beijing Institute of Control Engineering Beijing 100190Chin

Subpixel localization techniques for estimating the positions of point-like images captured by pixelated image sensors have been widely used in diverse optical measurement fields.With unavoidable imaging noise,there is a precision limit(PL)when estimating the target positions on image sensors,which depends on the detected photon count,noise,point spread function(PSF)radius,and PSF’s intra-pixel position.Previous studies have clearly reported the effects of the first three parameters on the PL but have neglected the intra-pixel position information.Here,we develop a localization PL analysis framework for revealing the effect of the intra-pixel position of small PSFs.To accurately estimate the PL in practical applications,we provide effective PSF(e PSF)modeling approaches and apply the Cramér–Rao lower bound.Based on the characteristics of small PSFs,we first derive simplified equations for finding the best PL and the best intra-pixel region for an arbitrary small PSF;we then verify these equations on real PSFs.Next,we use the typical Gaussian PSF to perform a further analysis and find that the final optimum of the PL is achieved at the pixel boundaries when the Gaussian radius is as small as possible,indicating that the optimum is ultimately limited by light diffraction.Finally,we apply the maximum likelihood method.Its combination with e PSF modeling allows us to successfully reach the PL in experiments,making the above theoretical analysis effective.This work provides a new perspective on combining image sensor position control with PSF engineering to make full use of information theory,thereby paving the way for thoroughly understanding and achieving the final optimum of the PL in optical localization.

关键词： Optical measurement Subpixel localization Precision limit optimization Small point spread functions Centroiding Star sensors

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