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| 1 | Interleukin-17 and its expanding biological functions显示文摘Interleukin-17(IL-17)and IL-17-producing cells have been shown to play important roles in inflammation and the immune response.IL-17 is believed to be mainly produced by T helper 17(Th17)cells,a unique helper T-cell subset different from Th1 and Th2 cells.Other subsets of T cells such as cdT and natural killer T(NKT)cells have also been found to produce IL-17 in response to innate stimuli.IL-17 acts as a proinflammatory cytokine that can induce the release of certain chemokines,cytokines,matrix metalloproteinases(MMPs)and antimicrobial peptides from mesenchymal and myeloid cells.This leads to the expansion and accumulation of neutrophils in the innate immune system and links innate and adaptive immunity in vivo.Furthermore,increasing evidence indicates that IL-17 and IL-17-producing cells are involved in the pathogenesis of various diseases such as allergies,autoimmune diseases,allograft transplantation and even malignancy.They may also play protective roles in host defense against infectious diseases and promote induction of cytotoxic T lymphocyte(CTL)responses against cancer.Targeting of the IL-17 axis is under investigation for the treatment of inflammatory disorders. | Sheng Xu Xuetao Cao | 2010 | Cellular & Molecular Immunology2010，7，3： | 50 |
| 2 | Regulation of Toll-like receptor signaling in innate immunity显示文摘Toll-like receptors sense invading pathogens by recognizing a wide variety of conserved pathogen-associated molecular patterns(PAMPs).The members of the TLR family selectively utilize adaptor proteins MyD88,TRIF,TIRAP and TRAM to activate overlapping but distinct signal transduction pathways which trigger production of different panels of mediators such as proinflammatory cytokines and type I interferon.These mediators not only control innate immunity but also direct subsequently developed adaptive immunity.TLR activation is strictly and finely regulated at multiple levels of the signal transduction pathways. | AN HuaZhang,QIAN Cheng & CAO XueTao National Key Laboratory of Medical Immunology & Institute of Immunology,Second Military Medical University,Shanghai 200433,China | 2010 | Science China(Life Sciences)2010，53，1： | 29 |
| 3 | The origin and function of tumor-associated macrophages显示文摘 | Yang Liu Xuetao Cao | 2015 | Cellular & Molecular Immunology2015，12，1： | 27 |
| 4 | Siglecl suppresses antiviral innate immune response by inducing TBK1 degradation via the ubiquitin ligase TRIM27显示文摘 | Qingliang Zheng Jin Hou Ye Zhou Yingyun Yang Bing Xie Xuetao Cao | 2015 | Cell Research2015，25，10： | 21 |
| 5 | Cellular and molecular regulation of innate inflammatory responses显示文摘由模式识别受体(PRR ) 的病原体的天生的察觉到在在自我和非自我部件之间的天生的辨别起必要作用,导致天生的有免疫力的防卫和煽动性的回答的产生。天生的煽动性的反应的开始,激活和分辨率被相互作用的一个复杂网络在有免疫力、非有免疫力的系统的众多的细胞、分子的部件之中调停。当时一控制并且有益的天生的煽动性的反应是批评的因为病原体的消除和织物动态平衡, dysregulated 或持续发炎的维护导致象长期的感染那样的病理学的条件,煽动性的自体免疫的疾病。在这评论,我们为天生的免疫和煽动性的回答的建立和规定在我们细胞、分子的机制的理解讨论一些最近的进展。 | Juan Liu Xuetao Cao | 2016 | Cellular & Molecular Immunology2016，13，6： | 20 |
| 6 | Immunosuppressive exosomes from TGF-pl gene-modified dendritic cells attenuate Th17-mediated inflammatory autoimmune disease by inducing regulatory T cells显示文摘 | Zhijian Cai Wei Zhang Fei Yang Lei Yu Zhou Yu JihHung Pan Lie Wang Xuetao Cao Jianli Wang | 2012 | Cell Research2012，22，3： | 20 |
| 7 | TGF-β1 gene-modified,immature dendritic cells delay the development of inflammatory bowel disease by inducing CD4^(+)Foxp3^(+)regulatory T cells显示文摘Inflammatory bowel disease(IBD)is caused by an uncontrolled immune response in the intestinal lumen,leading to inflammation in genetically predisposed individuals.Immunotherapy may be a promising approach to the treatment of IBD.Here,we show that transforming growth factor-β1(TGF-β1)gene-modified immature dendritic cells(imDCs)could enhance the inhibitory function of imDCs and delay the progress of IBD induced by dextran sodium sulfate in mice.The results of fluorescence-activated cell sorter(FACS)demonstrated that this protective effect is mediated partially by inducing CD4^(+)Foxp3^(+)regulatory T cells(Tregs)in mesentery lymph nodes to control inflammation.In vitro experiments also supported this hypothesis.In conclusion,we provide evidence that TGF-b1-modified bone marrow-derived imDCs may have a therapeutic effect to IBD. | Zhijian Cai Wei Zhang Min Li Yinpu Yue Fei Yang Lei Yu Xuetao Cao Jianli Wang | 2010 | Cellular & Molecular Immunology2010，7，1： | 18 |
| 8 | Reversing drug resistance of soft tumor-repopulating cells by tumor cell-derived chemotherapeutic microparticles显示文摘颠倒使人重新住入肿瘤的房间(TRC ) 的药抵抗或起源的发展中的新奇途径像房间的癌症房间是迫切临床的需要改进癌症病人的结果。这里,我们显示出用肿瘤颠倒 TRC 的药抵抗的一条创新途径包含反肿瘤药的导出房间的 microparticles (T-MPs ) 。由比区分的癌症房间更可变形的优点, TRC 优先地收起 T-MPs 在进入房间以后释放反肿瘤药,它接着导致 TRC 的死亡。内在的机制包括防碍药流出并且支持这些药的原子入口。我们的调查结果在用有希望的临床的应用程序颠倒 TRC 的药抵抗在 T-MPs 的举起和一条新奇途径的有效性表明肿瘤房间柔软的重要性。 | Jingwei Ma Yi Zhang Ke Tang Huafeng Zhang Xiaonan Yin Yong Li Pingwei Xu Yanling Sun Ruihua Ma Tiantian Ji Junwei Chen Shuang Zhang Tianzhen Zhang Shunqun Luo Yang Jin Xiuli Luo Chengyin Li Hongwei Gong Zhixiong Long Jinzhi Lu Zhuowei Hu Xuetao Cao Ning Wang Xiangliang Yang Bo Huang | 2016 | Cell Research2016，26，6： | 17 |
| 9 | Long noncoding RNAs in innate immunity显示文摘长 noncoding RNA (lncRNAs ) 被显示了通过不同机制在有免疫力的房间开发和有免疫力的回答起重要作用,例如剂量赔偿,印, enhancer 功能,和 transcriptional 规定。尽管大多数 lncRNAs 的功能是不清楚的,某 lncRNAs 被发现了经由蛋白质蛋白质相互作用的新方法控制 transcriptional 或天生、适应的有免疫力的回答的 post-transcriptional 规定或与 DNA 和 RNA 配对。有趣地,增加证据阐明了在在主人和病原体之间的相互作用的 lncRNAs 的重要性。在这评论,行动的 lncRNAs 模式的概述,以及在免疫的 lncRNAs 的重要、多样化的角色,被提供,并且在调整天生的有免疫力的回答的 lncRNAs 的一个新兴的范例被加亮。 | Yuan Zhang Xuetao Cao | 2016 | Cellular & Molecular Immunology2016，13，2： | 17 |
| 10 | Oral berberine improves brain dopa/dopamine levels to ameliorate Parkinson’s disease by regulating gut microbiota显示文摘The phenylalanine-tyrosine-dopa-dopamine pathway provides dopamine to the brain.Iin this process,tyrosine hydroxylase(TH)isthe rate-limiting enzyme that hydroxylates tyrosine and generates levodopa(L-dopa)with tetranydrobiopterin(BH_(4))as a coenzyme.Here,we show that oral berberine(BBR)might supply H^(·) through dihydroberberine(reduced BBR produced by bacterial nitroreductase)and promote the production of BHl from dihydrobiopterin;the increased BH,enhances TH activity,which accelerates the production of L-dopa by the gut bacteria.Oral BBR acts in a way similar to vitamins.The L-dopa produced by theintestinal bacteria enters the brain through the circulation and is transformed to dopamine.To verify the gut-brain dialog activatedby BBR's effect,Enterococcus foecalis or Enterococcus faecium was transplanted into Parkinson's disease(PD)mice.The bacteriasignificantly increased brain dopamine and ameliorated PD manifestation in mice;additionally,combination of BBR with bacteriashowed better therapeutic effect than that with bacteria alone.Moreover,2,4,6-trimethy-pyranylium tetrafluoroborate(TMP-TFB)-derivatized matrix-assisted laser desorption mass spectrometry(MALDI-MS)imaging of dopamine identihed elevated striataldopamine levels in mouse brains with oral Enterococcus,and BBR strengthened the imaging intensity of brain dopamine.Theseresults demonstrated that BBR was an agonist of TH in Enterococcus and could lead to the production of L-dopa in the gut.Furthermore,a study of 28 patients with hyperlipidemia conhrmed that oral BBR increased bloodfecal L-dopa by the intestinalbacteria.Hence,BBR might improve the brain function by upregulating the biosynthesis of-dopa in the gut microbiota through avitamin-like effect. | Yan Wang Qian Tong Shu-Rong Ma Zhen-Xiong Zhao Li-Bin Pan Lin Cong Pei Han Ran Peng Hang Yu Yuan Lin Tian-Le Gao Jia-Wen Shou Xiao-Yang Li Xian-Feng Zhang Zheng-Wei Zhang Jie Fu Bao-Ying Wen Jin-Bo Yu Xuetao Cao Jian-Dong Jiang | 2021 | Signal Transduction and Targeted Therapy2021，6，3： | 16 |
| 11 | Low-dose decitabine enhances the effect of PD-1 blockade in colorectal cancer with microsatellite stability by re-modulating the tumor microenvironment显示文摘PD-1 blockade has demonstrated impressive clinical outcomes in colorectal cancers that have high microsatellite instability.However,the therapeutic efficacy for patients with tumors with low microsatellite instability or stable microsatellites needs further improvement.Here,we have demonstrated that low-dose decitabine could increase the expression of immune-related genes such as major histocompatibility complex genes and cytokine-related genes as well as the number of lymphocytes at the tumor site in CT26 colorectal cancer-bearing mice.A more significant inhibition of tumor growth and a prolongation of survival were observed in the CT26 mouse model after treatment with a combination of PD-1 blockade and decitabine than in mice treated with decitabine or PD-1 blockade alone.The anti-tumor effect of the PD-1 blockade was enhanced by low-dose decitabine.The results of RNA sequencing and whole-genome bisulfite sequencing of decitabine-treated CT26 cells and tumor samples with microsatellite stability from the patient tumor-derived xenograft model have shown that many immune-related genes,including antigen-processing and antigen-presenting genes,were upregulated,whereas the promoter demethylation was downregulated after decitabine exposure.Therefore,decitabine-based tumor microenvironment re-modulation could improve the effect of the PD-1 blockade.The application of decitabine in PD-1 blockade-based immunotherapy may elicit more potent immune responses,which can provide clinical benefits to the colorectal cancer patients with low microsatellite instability or stable microsatellites. | Ganjun Yu Yanfeng Wu Wenying Wang Jia Xu Xiaoping Lv Xuetao Cao Tao Wan | 2019 | Cellular & Molecular Immunology2019，16，4： | 14 |
| 12 | TLR4 is essential for dendritic cell activation and anti-tumor T-cell response enhancement by DAMPs released from chemically stressed cancer cells显示文摘免疫疗法和化疗的联合为癌症的某些类型的治疗被认为是一条有希望的途径。然而,内在的机制需要充分被调查为癌症 chemoimmunotherapy 指导更有效的协议的设计。联系危险的分子的模式(阻尼) 能激活有免疫力的房间,是众所周知的,包括树枝状的房间(DC ) ,经由像使用费的受体(TLR ) ;然而,在有免疫力的反应的激活免除化学对待药的肿瘤房间的阻尼的角色需要进一步被阐明。这里,我们发现那 colorectal 与 oxaliplatin (OXA ) 对待的癌症(CRC ) 房间或 5 氟尿嘧啶(5-Fu ) 释放了高活动性的组盒子 1 的高水平(HMGB1 ) 和热吃惊蛋白质 70 (HSP70 ) 。在 OXA/5-Fu 治疗以后,也展出的 CRC 病人的 sera 增加了 HMGB1 和 HSP70 的层次,哪个是著名阻尼。与 OXA/5-Fu 对待的垂死的 CRC 房间的上层清液支持了老鼠和人的 DC 成熟,与 HLA 医生, CD80 和 CD86 表示和 IL-1β 的改进的 upregulation;, TNF-α, MIP-1α, MIP-1β, RANTES 和 IP-10 生产。由 DC 组成的疫苗与导致的化学上强调的 CRC 房间的上层清液搏动了更重要的 IFN-γ在 vitro 并且在 vivo 生产 Th1 反应。然而,化学上强调的 CRC 房间的上层清液没能在 TLR4 缺乏的 DC 导致 phenotypic 成熟和 cytokine 生产,显示在导致阻尼的 DC 成熟和激活的 TLR4 的一个必要角色。而且,有化学上强调的 CRC 房间的上层清液的 pulsing 高效地没导致 IFN-γ在 TLR4 缺乏的 DC 生产 Th1 反应。一起,这些结果证明免除化学上强调的癌症房间的阻尼能经由 TLR4 激活 DC 并且提高反肿瘤 T 房间有免疫力的回答的正式就职,描出一条临床上相关的免疫助手小径由阻尼被触发。 | Hongliang Fang Bing Ang Xinyun Xu Xiaohui Huang Yanfeng Wu Yanping Sun Wenying Wang Nan Li Xuetao Cao Tao Wan | 2014 | Cellular & Molecular Immunology2014，11，2： | 11 |
| 13 | Organotropic metastasis: role of tumor exosomes显示文摘 | Yang Liu Xuetao Cao | 2016 | Cell Research2016，26，2： | 11 |
| 14 | MicroRNA in vivo precipitation identifies miR-151-3p as a computational unpredictable miRNA to target Stat3 and inhibits innate IL-6 production显示文摘MicroRNAs(miRNAs)function as important regulators in the immune response and inflammation.Several approaches have been reported to computationally predict miRNAs and their potential targets.However,there are still many miRNA–target interactions that are unpredictable by using the current computational algorithms.We established a miRNA in vivo precipitation method(miRIP)to identify unpredictable miRNAs with definite targets in these cells.Because Stat3 is a well-known transcription factor involved in innate immunity and inflammation,we utilized the miRIP method to identify miRNAs that bind Stat3 mRNA in macrophages.Among the captured miRNAs,miR-151-3p was confirmed to interact with Stat3 mRNA 3′-UTR and downregulate the Stat3 protein levels.LPS stimulation decreased miR-151-3p expression,thereby increasing IL-6 production.Therefore,we found that miR-151-3p inhibited LPS-induced IL-6 production by targeting Stat3.These data further confirmed miRIP as an efficient method to identify unpredictable miRNAs and explore miRNAs-mediated regulation in innate immunity and inflammation. | Xiang Liu Xiaoping Su Sheng Xu Huamin Wang Dan Han Jiangxue Li Mingyan Huang Xuetao Cao | 2018 | Cellular & Molecular Immunology2018，15，2： | 8 |
| 15 | Dendritic cell migration in inflammation and immunity显示文摘Dendritic cells(DCs)are the key link between innate immunity and adaptive immunity and play crucial roles in both the promotion of immune defense and the maintenance of immune tolerance.The trafficking of distinct DC subsets across lymphoid and nonlymphoid tissues is essential for DC-dependent activation and regulation of inflammation and immunity.DC chemotaxis and migration are triggered by interactions between chemokines and their receptors and regulated by multiple intracellular mechanisms,such as protein modification,epigenetic reprogramming,metabolic remodeling,and cytoskeletal rearrangement,in a tissue-specific manner.Dysregulation of DC migration may lead to abnormal positioning or activation of DCs,resulting in an imbalance of immune responses and even immune pathologies,including autoimmune responses,infectious diseases,allergic diseases and tumors.New strategies targeting the migration of distinct DC subsets are being explored for the treatment of inflammatory and infectious diseases and the development of novel DC-based vaccines.In this review,we will discuss the migratory routes and immunological consequences of distinct DC subsets,the molecular basis and regulatory mechanisms of migratory signaling in DCs,and the association of DC migration with the pathogenesis of autoimmune and infectious diseases. | Juan Liu Xiaomin Zhang Yujie Cheng Xuetao Cao | 2021 | Cellular & Molecular Immunology2021，18，11： | 8 |
| 16 | Interferon-inducible cytoplasmic lncLrrc55-AS promotes antiviral innate responses by strengthening IRF3 phosphorylation显示文摘Type I interferon (IFN-I) production is efficiently induced to ensure a potent innate immune response to viral infection. How this response can be enhanced, however, remains to be explored. Here, we identify a new cytoplasmic long non-coding RNA (lncRNA), lncLrrc55-AS, that drives a positive feedback loop to promote interferon regulatory factor 3 (IRF3) signaling and IFN-I production. We show that lncLrrc55-AS is virus-induced in multiple cell types via the IFN-JAK-STAT pathway. LncLrrc55-AS-deficient mice display a weakened antiviral immune response and are more susceptible to viral challenge. Mechanistically, lncLrrc55-AS binds phosphatase methylesterase 1 (PME-1), and promotes the interaction between PME-1 and the phosphatase PP2A, an inhibitor of IRF3 signaling. LncLrrc55-AS supports PME-1-mediated demethylation and inactivation of PP2A, thereby enhancing IRF3 phosphorylation and signaling. Loss of PME-1 phenocopies lncLrrc55-AS deficiency, leading to diminished IRF3 phosphorylation and IFN-I production. We have identified an IFN-induced lncRNA as a positive regulator of IFN-I production, adding mechanistic insight into lncRNA-mediated regulation of signaling in innate immunity and inflammation. | Yumei Zhou Mengxuan Li Yiquan Xue Zhiqing Li Weitao Wen Xingguang Liu Yuanwu Ma Lianfeng Zhang Zhongyang Shen Xuetao Cao | 2019 | Cell Research2019，29，8： | 8 |
| 17 | LR members in inflammation-associated arcinogenesis显示文摘 | Ha Zhu Xuetao Cao | 2017 | Cellular & Molecular Immunology2017，14，5： | 7 |
| 18 | The function and regulation of TET2 in innate immunity and inflammation显示文摘TET2,a member of ten-eleven translocation(TET)family as a-ketoglutarate-and Fe2+-dependent dioxygenase catalyzing the iterative oxidation of 5-methylcytosine(5mC),has been widely recognized to be an important regulator for normal hematopoiesis especially myelopoiesis.Mutation and dysregulation of TET2 contribute to the development of multiple hematological malignancies.Recent studies reveal that TET2 also plays an important role in innate immune homeostasis by promoting DNA demethylation or independent of its enzymatic activity.Here,we focus on the functions of TET2 in the initiation and resolution of inflammation through epigenetic regulation and signaling network.In addition,we highlight regulation of TET2 at various molecular levels as well as the correlated inflammatory diseases,which will provide the insight to intervene in the pathological process caused by TET2 dysregulation. | Boyi Cong Qian Zhang Xuetao Cao | 2021 | Protein & Cell2021，12，3： | 6 |
| 19 | Highlights of the advances in basic immunology in 2011显示文摘在这评论,我们在研究在 2011 报导了的免疫学的总结主要基本进展。热点集中于关键问题的改进理解在基本免疫学,包括象为各种各样的 T 房间子集的开发和函数的机制一样的天生的回答的开始和激活。研究象像使用费的受体(TLR ) 和 retinoic 的新奇管理者的鉴定一样包括新奇 cytosolic RNA 和 DNA 传感器的鉴定酸可诱导的基因(RIG-I ) 我喜欢发信号的受体(RLR ) 小径。而且,显著进展在天生的淋巴的房间(ILC ) 的发展、功能的性质被做了。助手 T 房间和规章的 T (Treg ) 房间在安排适应免疫起不可缺少的作用。在那里关于不同 T 房间子集的发展的规章的机制使发现一直在激动,特别地 Th17 房间和 Treg 房间。在 T 房间免疫的 microRNAs (miRNAs ) 的新兴的角色被讨论,作为一个新奇 T 房间子集的最近的鉴定被叫作小囊的规章的 T (TFR ) 房间。 | Juan Liu Shuxun Liu Xuetao Cao | 2012 | Cellular & Molecular Immunology2012，9，3： | 6 |
| 20 | Activated cytotoxic lymphocytes promote tumor progression by increasing the ability of 3LL tumor cells to mediate MDSC chemoattraction via Fas signaling显示文摘Fas/FasL 系统播送细胞内部的 apoptotic 发信号,导致房间 apoptosis。然而,船边交货发信号也除了导致肿瘤房间 apoptosis 施加 non-apoptotic 功能。例如,船边交货发信号导致肺癌症肿瘤房间生产前列腺素 E2 (PGE2 ) 和成员导出 myeloid 的 suppressor 房间(MDSC ) 。激活的细胞毒素的 T 淋巴细胞(CTL ) 导致并且表示 FasL 在房间仍然是的 apoptosis 抵抗的肿瘤上在 CTL 开始的船边交货激活的 FasL,而是效果的高水平大部分不清楚。我们从 OT-1 老鼠净化了激活的 CD8 + T 房间,在肿瘤房间逃跑上评估了船边交货激活的规章的效果并且调查了相关机制。我们发现 CTL 导致了肿瘤细胞分泌 PGE2 和增加肿瘤经由船边交货发信号的 MDSC 的调停房间的 chemoattraction,它对肿瘤生长有利。我们的结果显示 CTL 可以参予肿瘤免疫者避免过程。就我们的知识而言,这是 CTL 在肿瘤逃跑由起一个作用的新奇机制。我们的调查结果含有经由对肿瘤的否定有免疫力的回答的减小提高 antitumor 免疫者反应的策略通过船边交货发信号由 CTL 支持了。 | Fei Yang Yinxiang Wei Zhijian Cai Lei Yu Lingling Jiang Chengyan Zhang Huanmiao Yan Qingqing Wang Xuetao Cao Tingbo Liang Jianli Wang | 2015 | Cellular & Molecular Immunology2015，12，1： | 6 |
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