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| 1 | Molecular mechanisms regulating NLRP3 inflammasome activation显示文摘Inflammasomes 是表明触发煽动性的 caspases 的激活和 interleukin-1β 的成熟的建筑群的多蛋白质;。在各种各样的 inflammasome 建筑群之中, NLRP3 inflammasome 最好被描绘并且与各种各样的人的 autoinflammatory 和自体免疫的疾病被连接了。因此, NLRP3 inflammasome 可以是为反煽动性的治疗的一个有希望的目标。在这评论,我们总结 NLRP3 inflammasome 被在 cytosol 激活的机制的当前的理解。我们也描述激活或禁止 inflammasome 汇编的 NLRP3 inflammasome 建筑群的有约束力的搭挡。我们调整 NLRP3 inflammasome 发信号的机制的知识并且这些怎么影响煽动性的回答,提供进一步的卓见进潜在的治疗学的策略治疗与 NLRP3 inflammasome 的 dysregulation 联系的煽动性的疾病。 | Eun-Kyeong Jo Jin Kyung Kim Dong-Min Shin Chihiro Sasakawa | 2016 | Cellular & Molecular Immunology2016，13，2： | 202 |
| 2 | Necroptosis, pyroptosis and apoptosis: an intricate game of cell death显示文摘Cell death is a fundamental physiological process in all living organisms.Its roles extend from embryonic development,organ maintenance,and aging to the coordination of immune responses and autoimmunity.In recent years,our understanding of the mechanisms orchestrating cellular death and its consequences on immunity and homeostasis has increased substantially.Different modalities of what has become known as‘programmed cell death’have been described,and some key players in these processes have been identified.We have learned more about the intricacies that fine tune the activity of common players and ultimately shape the different types of cell death.These studies have highlighted the complex mechanisms tipping the balance between different cell fates.Here,we summarize the latest discoveries in the three most well understood modalities of cell death,namely,apoptosis,necroptosis,and pyroptosis,highlighting common and unique pathways and their effect on the surrounding cells and the organism as a whole. | Damien Bertheloot Eicke Latz Bernardo S.Franklin | 2021 | Cellular & Molecular Immunology2021，18，5： | 84 |
| 3 | NLRP3 inflammasome activation and cell death显示文摘The NLRP3 inflammasome is a cytosolic multiprotein complex composed of the innate immune receptor protein NLRP3,adapter protein ASC,and inflammatory protease caspase-1 that responds to microbial infection,endogenous danger signals,and environmental stimuli.The assembled NLRP3 inflammasome can activate the protease caspase‐1 to induce gasdermin D-dependent pyroptosis and facilitate the release of IL-1β and IL-18,which contribute to innate immune defense and homeostatic maintenance.However,aberrant activation of the NLRP3 inflammasome is associated with the pathogenesis of various inflammatory diseases,such as diabetes,cancer,and Alzheimer’s disease.Recent studies have revealed that NLRP3 inflammasome activation contributes to not only pyroptosis but also other types of cell death,including apoptosis,necroptosis,and ferroptosis.In addition,various effectors of cell death have been reported to regulate NLRP3 inflammasome activation,suggesting that cell death is closely related to NLRP3 inflammasome activation.In this review,we summarize the inextricable link between NLRP3 inflammasome activation and cell death and discuss potential therapeutics that target cell death effectors in NLRP3 inflammasome-associated diseases. | Yi Huang Wen Xu Rongbin Zhou | 2021 | Cellular & Molecular Immunology2021，18，9： | 94 |
| 4 | Nuclear Factor-κB:Activation and Regulation during Toll-Like Receptor Signaling显示文摘Toll-like receptors (TLRs) recognize distinct microbial components to initiate the innate and adaptive immune responses. TLR activation culminates in the expression of appropriate pro-inflammatory and immunomodulatory factors to meet pathogenic challenges. The transcription factor NF-κB is the master regulator of all TLR-induced responses and its activation is the pivotal event in TLR-mediated activation of the innate immune response. Many of the key molecular events required for TLR-induced NF-κB activation have been elucidated. However, much remain to be learned about the ability of TLRs to generate pathogen-specific responses using a limited number of transcription factors. This review will focus on our current understanding of NF-κB activation by TLRs and potential mechanisms for achieving a signal-specific response through NF-κB. | Ruaidhrí J. Carmody | 2007 | Cellular & Molecular Immunology2007，4，1： | 63 |
| 5 | NK cell-based immunotherapy for malignant diseases显示文摘生来的杀手(NK ) 房间对癌症在主人免疫起关键作用。在反应,癌症开发机制逃离 NK 房间攻击或导致有缺点的 NK 房间。当前的 NK 基于房间的癌症免疫疗法试图用几条途径克服 NK 房间麻痹。一条途径使用扩展 allogeneic NK 房间,它没被象自体同源的 NK 房间一样的自我 histocompatibility 抗原禁止,为采纳细胞的免疫疗法。另一条采纳转移途径使用稳定的 allogeneic NK 房间线,它为质量控制和大规模生产是更实际的。第三条途径是新鲜 NK 房间或 NK 房间线的基因修正高度表示 cytokines, Fc 受体或妄想的肿瘤抗原受体。治疗学的 NK 细胞能从各种各样的来源被导出,包括细胞,干细胞或甚至导致的 pluripotent 干细胞( iPSCs ),和许多激发器能被用于的外设或绳索血在实验室或好生产实践( GMP )的大规模生产设备包括可溶的生长因素,使不能调动的分子或抗体,和另外的细胞的使活跃之物。到在临床的试用的癌症的对待几类型的 NK 房间治疗的一张表这里被考察。基于 NK 的免疫疗法的几条不同途径例如织物特定的 NK 房间,漂亮面向受体的 NK 房间和化学上对待的 NK 房间,被讨论。一些新技术或策略到由非侵略的成像的监视器 NK 房间治疗,预定 NK 房间治疗由的效率在 vivo 实验并且在临床的试用评估 NK 房间治疗途径也被介绍。 | Min Cheng Yongyan Chen Weihua Xiao Rui Sun Zhigang Tian | 2013 | Cellular & Molecular Immunology2013，10，3： | 61 |
| 6 | The cytokine storm of severe influenza and development of immunomodulatory therapy显示文摘严重流行性感冒为人在它的毒力仍然保持不平常。复杂并发症或最终,从这些感染产生的死亡经常与 proinflammatory cytokine 生产的 hyperinduction 被联系,它也作为 ‘ 被知道; cytokine storm’。为这疾病, immunomodulatory 治疗可以改进结果,这被建议了,与或没有抗病毒的代理人的联合。这里,我们考察免疫系统的各种各样的受动器怎么开始 cytokine 暴风雨并且在主人加重病理学的损坏的当前的文学。我们也在严重流行性感冒为 cytokine 暴风雨的治疗考察一些当前的 immunomodulatory 策略,包括 corticosteroids , peroxisome 激活proliferator 的受体收缩筋, sphingosine-1-phosphate 受体 1 收缩筋, cyclooxygenase-2 禁止者,抗氧化剂, anti-tumour-necrosis 因素治疗,静脉内的免疫球蛋白治疗, statins , arbidol ,植物,并且另外的潜在的治疗学的策略。 | Qiang Liu Yuan-hong Zhou Zhan-qiu Yang | 2016 | Cellular & Molecular Immunology2016，13，1： | 72 |
| 7 | Liver immunology and its role in inflammation and homeostasis显示文摘当一个非免疫学的机关首先从事了新陈代谢的、滋养的存储和 detoxification 活动,人的肝通常被察觉。然而,我们现在知道健康的肝也是复杂免疫学的一个地点活动象非造血的房间人口一样由一个多样的有免疫力的房间全部剧目调停了。在疾病得非的肝,新陈代谢并且织物改变功能要求发炎的元素。在有到饮食、微生物引起的产品的常规暴露的联合,这发炎为过多的有免疫力的激活创造潜力。在这复杂微型环境,肝的免疫系统容忍无害的分子当同时对可能的传染代理人仍然保持警惕时,恶意的房间或纸巾损坏。在到由病原体或织物损坏的挑战的适当有免疫力的激活之上,解决发炎的机制是必要的维持肝动态平衡。清除 ‘ 的失败; dangerous’刺激或调整适当地激活的有免疫力的机制导致病理学的发炎和纤维变性,肝硬化和最终的肝失败的进步发展描绘的破坏织物动态平衡。肝的煽动性的机制因此在健康的成年的肝有角色的一个系列;他们是必要的维持织物和机关动态平衡并且 dysregulated,肝病理的关键司机与长期的感染, autoimmunity 和恶意被联系。在这评论,我们在正常的肝动态平衡探索发炎和煽动性的调停人的变化感觉并且求婚作为一条治疗学的途径肝特定的有免疫力的规定小径指向治疗肝疾病。 | Mark W Robinson Cathal Harmon Cliona O'Farrelly | 2016 | Cellular & Molecular Immunology2016，13，3： | 65 |
| 8 | The history and advances in cancer immunotherapy:understanding the characteristics of tumor-infiltrating immune cells and their therapeutic implications显示文摘Immunotherapy has revolutionized cancer treatment and rejuvenated the field of tumor immunology.Several types of immunotherapy,including adoptive cell transfer(ACT)and immune checkpoint inhibitors(ICIs),have obtained durable clinical responses,but their efficacies vary,and only subsets of cancer patients can benefit from them.Immune infiltrates in the tumor microenvironment(TME)have been shown to play a key role in tumor development and will affect the clinical outcomes of cancer patients.Comprehensive profiling of tumor-infiltrating immune cells would shed light on the mechanisms of cancer–immune evasion,thus providing opportunities for the development of novel therapeutic strategies.However,the highly heterogeneous and dynamic nature of the TME impedes the precise dissection of intratumoral immune cells.With recent advances in single-cell technologies such as single-cell RNA sequencing(scRNA-seq)and mass cytometry,systematic interrogation of the TME is feasible and will provide insights into the functional diversities of tumor-infiltrating immune cells.In this review,we outline the recent progress in cancer immunotherapy,particularly by focusing on landmark studies and the recent single-cell characterization of tumor-associated immune cells,and we summarize the phenotypic diversities of intratumoral immune cells and their connections with cancer immunotherapy.We believe such a review could strengthen our understanding of the progress in cancer immunotherapy,facilitate the elucidation of immune cell modulation in tumor progression,and thus guide the development of novel immunotherapies for cancer treatment. | Yuanyuan Zhang Zemin Zhang | 2020 | Cellular & Molecular Immunology2020，17，8： | 61 |
| 9 | Transplantation of Human Bone Marrow Mesenchymal Stem Cell Ameliorates the Autoimmune Pathogenesis in MRL/lpr Mice显示文摘Recent evidence indicates that mesenchymal stem cells (MSC) possess immunosuppressive properties both in vitro and in vivo. We previously demonstrated the functional abnormality of bone marrow derived MSC in patients with systemic lupus erythematosus (SLE). In this study, we aimed to investigate whether transplantation of human bone marrow derived MSC affects the autoimmune pathogenesis in MRL/lpr mice. We found that human MSC from healthy donors reduced the proliferation of T lymphocytes from MRL/lpr mice in a dose-dependent fashion. Two weeks after in vivo transfer of MSC, we detected significantly reduced serum levels of anti ds-DNA antibodies and 24 hour proteinuria in MRL/lpr mice as compared with control groups without MSC transplantation. Moreover, flow cytometric analysis revealed markedly reduced number of CD4+ T cells while increased Th1 subpopulation in MSC group and MSC + CTX group when compared with controls. Histopathological examination showed significantly reduced renal pathology in MSC-treated mice. Immunohistochemical studies further revealed reduced expression of TGF-β, FN, VEGF and the deposition of complement C3 in renal tissue after MSC and MSC + CTX treatment. Taken together, we have demonstrated that transplantation of human MSC can significantly inhibit the autoimmune progression in MRL/lpr mice. | Kangxing Zhou Huayong Zhang Ouyang Jin Xuebing Feng Genhong Yao Yayi Hou Lingyun Sun | 2008 | Cellular & Molecular Immunology2008，5，6： | 59 |
| 10 | NK cell receptor imbalance and NK cell dysfunction in HBV nfection and hepatocellular carcinoma显示文摘Hepatocellular 癌(HCC ) 当前由于手术后的复发和转移是癌症死亡和普通差预后的恶意的第三个领先的原因。在长期的肝炎 B 之间有重要关联病毒(HBV ) 感染和 hepatocarcinogenesis。作为对病毒的感染和肿瘤的宿主防卫的第一根线,生来的杀手( NK )细胞表示很多有免疫力的识别受体( NK 受体( NKR ))在 hepatocytes ,肝正弦曲线 endothelial 细胞,星形的细胞和 Kupffer 细胞上认出 ligands ,它维持在有免疫力的反应和 NK 细胞的有免疫力的忍耐之间的平衡。不幸地,百分比和肝 NK 房间的绝对数字在 HCC 的发展和前进期间显著地减少。NK 房间受体和肝 NK 房间的机能障碍的反常表示贡献长期的 HBV 感染和 HCC 的前进并且显著地为肝癌症与差的预后被联系。在这评论,我们在 HCC 在反肿瘤免疫者回答集中于 NK 房间受体的角色,特别地 HBV 相关的 HCC。我们明确地讨论肿瘤房间怎么从 NK 房间躲避攻击并且 NKR 的新兴的理解怎么可以为 HCC 帮助新奇治疗的发展。小说单音 -- 并且指向 NK 房间 receptor-ligand 系统的治疗学的策略可以潜在地导致的联合在 HCC 的成功、有效的免疫疗法。 | Cheng Sun Haoyu Sun Cai Zhang Zhigang Tian | 2015 | Cellular & Molecular Immunology2015，12，3： | 55 |
| 11 | Hepatic macrophages in homeostasis and liver diseases: from pathogenesis to novel therapeutic strategies显示文摘巨噬细胞代表天生的免疫的一种主要房间类型并且在许多长期的煽动性的疾病作为一个批评播放器和治疗学的目标出现了。肝的巨噬细胞由 Kupffer 房间组成,它从胎儿的蛋黄麻袋被发源,并且渗入了骨头导出髓的单核白血球 / 巨噬细胞。肝的巨噬细胞在维持肝并且在肝损害的致病的动态平衡起一个中央作用,使他们成为为肝疾病的一个吸引人的治疗学的目标。然而,肝的巨噬细胞的各种各样的人口显示不同显型并且施加不同函数。因此,更多的研究被要求更好理解这些房间指导基于巨噬细胞的治疗学的干预的发展。这篇评论文章将在支持并且解决肝发炎,损害,和纤维变性在肝的巨噬细胞,他们在维持肝的动态平衡的功能,和他们的参与的起源和作文上总结当前的知识。最后,当前的策略正在被开发指向肝的巨噬细胞因为肝疾病的处理将被考察。 | Cynthia Ju Frank Tacke | 2016 | Cellular & Molecular Immunology2016，13，3： | 54 |
| 12 | Functional exhaustion of antiviral lymphocytes in COVID-19 patients显示文摘In December 2019,a novel coronavirus was first reported in Wuhan,China.1 It was named by the World Health Organization as severe acute respiratory syndrome coronavirus 2(SARS-CoV-2)and is responsible for coronavirus disease 2019(COVID-19).Up to 28 February 2020,79,394 cases have been confirmed according to China’s National Health Commission.Outside China,the virus has spread rapidly to over 36 countries and territories. | Yuanhong Xuand Zhigang Tian Meijuan Zheng Yong Gao Gang Wang Guobin Song Siyu Liu Dandan Sun Yuanhong Xu Zhigang Tian | 2020 | Cellular & Molecular Immunology2020，17，5： | 54 |
| 13 | NF-κB Signaling Pathway, Inflammation and Colorectal Cancer显示文摘 | Soly Wang Zhanjie Liu Lunshan Wang Xiaoren Zhang | 2009 | Cellular & Molecular Immunology2009，6，5： | 46 |
| 14 | New insights of T cells in the pathogenesis of psoriasis显示文摘干癣是 hyperproliferative keratinocytes 和 T 房间,树枝状的房间,巨噬细胞和 neutrophils 的渗入描绘的最普通的调停免疫者的长期的、煽动性的皮肤病之一。尽管干癣的致病充分没被理解,有宽大的证据,建议在皮肤的有免疫力的房间的 dysregulation,特别地 T 房间,在干癣开发起一个关键作用。在这评论,我们主要集中于病原的 T 房间并且讨论这些 T 房间怎么被激活并且在疾病致病包含了。最新识别的 ‘ professional’IL-17-producing 真皮的 γ δ在干癣的 T 房间和他们的潜在的角色将也被包括。最后,我们将简短为干癣处理在 T 房间和它的相关指向 cytokine 的治疗上总结最近的进步。 | Yihua Cai Chris Fleming Jun Yan | 2012 | Cellular & Molecular Immunology2012，9，4： | 49 |
| 15 | The regulation of the Treg/Th 17 balance by mesenchyma stem cells in human systemic lupus erythematosus显示文摘 | Dandan Wang Saisai Huang Xinran Yuan Jun Liang Renju Xu Genhong Yao Xuebing Feng Lingyun Sun | 2017 | Cellular & Molecular Immunology2017，14，5： | 44 |
| 16 | Exosomes mediate hepatitis B virus (HBV) transmission and NK-cell dysfunction显示文摘证据建议 exosomes 能转移在房间之间的基因材料。然而,他们在肝炎 B 的角色病毒(HBV ) 感染遗体不清楚。这里,我们报导在长期的肝炎 B (CHB ) 病人的 sera 在场的 exosomes 包含了两 HBV nucleic 酸和 HBV 蛋白质,并且以一种活跃方式把 HBV 转移了到 hepatocytes。尤其是, HBV nucleic 酸在生来的杀手(NK ) 被检测从在到 HBV 积极的 exosomes 的暴露以后的 CHB 病人和健康施主的房间。通过即时荧光显微镜学和流动 cytometry, 1,1-dioctadecyl-3,3,3,3, -tetramethylindodicarbocyanine, 4-chlorobenzenesulfnate 盐() 标记的 exosomes 被观察与 NK 房间交往并且被 NK 房间收起,它被转变生长因素提高 -- 治疗。而且, HBV 积极的 exosomes 损害了 NK 房间功能,包括干扰素(IFN )- 生产, cytolytic 活动, NK 房间增长和幸存,以及房间到的应答 poly (我: C ) 刺激。HBV 感染压制了模式识别受体的表示,特别 retinoic 酸可诱导的基因我(RIG-I ) 在 NK 房间上,导致原子因素 B (NF-B ) 和 p38 阻抑激活 mitogen 的蛋白质 kinase 小径。我们的结果在 CHB 感染期间在 HBV 传播和 NK 房间机能障碍加亮 exosomes 的一个以前未得到欣赏的角色。 | Yinli Yang Qiuju Han Zhaohua Hou Cai Zhang Zhigang Tian Jian Zhang | 2017 | Cellular & Molecular Immunology2017，14，5： | 47 |
| 17 | Innate immunity in tuberculosis: host defense vs pathogen evasion显示文摘The major innate immune cell types involved in tuberculosis(TB)infection are macrophages,dendritic cells(DCs),neutrophils and natural killer(NK)cells.These immune cells recognize the TB-causing pathogen Mycobacterium tuberculosis(Mtb)through various pattern recognition receptors(PRRs),including but not limited to Toll-like receptors(TLRs),Nod-like receptors(NLRs)and C-type lectin receptors(CLRs).Upon infection by Mtb,the host orchestrates multiple signaling cascades via the PRRs to launch a variety of innate immune defense functions such as phagocytosis,autophagy,apoptosis and inflammasome activation.In contrast,Mtb utilizes numerous exquisite strategies to evade or circumvent host innate immunity.Here we discuss recent research on major host innate immune cells,PRR signaling,and the cellular functions involved in Mtb infection,with a specific focus on the host’s innate immune defense and Mtb immune evasion.A better understanding of the molecular mechanisms underlying host–pathogen interactions could provide a rational basis for the development of effective anti-TB therapeutics. | Cui Hua Liu Haiying Liu Baoxue Ge | 2017 | Cellular & Molecular Immunology2017，14，12： | 43 |
| 18 | The role of gut microbiota(commensal bacteria)and the mucosal barrier in the pathogenesis of inflammatory and autoimmune diseases and cancer:contribution of germ-free and gnotobiotic animal models of human diseases显示文摘Metagenomic approaches are currently being used to decipher the genome of the microbiota(microbiome),and,in parallel,functional studies are being performed to analyze the effects of the microbiota on the host.Gnotobiological methods are an indispensable tool for studying the consequences of bacterial colonization.Animals used as models of human diseases can be maintained in sterile conditions(isolators used for germ-free rearing)and specifically colonized with defined microbes(including non-cultivable commensal bacteria).The effects of the germ-free state or the effects of colonization on disease initiation and maintenance can be observed in these models.Using this approach we demonstrated direct involvement of components of the microbiota in chronic intestinal inflammation and development of colonic neoplasia(i.e.,using models of human inflammatory bowel disease and colorectal carcinoma).In contrast,a protective effect of microbiota colonization was demonstrated for the development of autoimmune diabetes in non-obese diabetic(NOD)mice.Interestingly,the development of atherosclerosis in germ-free apolipoprotein E(ApoE)-deficient mice fed by a standard low-cholesterol diet is accelerated compared with conventionally reared animals.Mucosal induction of tolerance to allergen Bet v1 was not influenced by the presence or absence of microbiota.Identification of components of the microbiota and elucidation of the molecular mechanisms of their action in inducing pathological changes or exerting beneficial,disease-protective activities could aid in our ability to influence the composition of the microbiota and to find bacterial strains and components(e.g.,probiotics and prebiotics)whose administration may aid in disease prevention and treatment. | Helena Tlaskalova-Hogenova Renata Stepankova Hana Kozakova Tomas Hudcovic Luca Vannucci Ludmila Tuckova Pavel Rossmann TomasHrncır Miloslav Kverka Zuzana Zakostelska Klara Klimesova Jaroslava Pribylova Jirina Bartova Daniel Sanchez Petra Fundova Dana Borovska Dagmar Sru˚tkova Zdenek Zıdek Martin Schwarzer Pavel Drastich David P Funda | 2011 | Cellular & Molecular Immunology2011，8，2： | 47 |
| 19 | 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 |
| 20 | Programmed death-1 upregulation is correlated with dysfunction of tumor-infiltrating CD8^(+ ) T lymphocytes in human non-small cell lung cancer显示文摘T-cell tolerance is an important mechanism for tumor escape,but the molecular pathways involved in T-cell tolerance remain poorly understood.It remains unknown whether the inhibitory immunoreceptor programmed death-1(PD-1)plays a role in conditions of human non-small cell lung cancer(NSCLC).In this study,we detected PD-1 expression on CD81 T cells from healthy control peripheral blood mononuclear cells(PBMCs)and the PBMCs of NSCLC patients as well as NSCLC tissues.Results showed that tumor-infiltrating CD81 T cells had increased PD-1 expression and impaired immune function,including reducing cytokine production capability and impairing capacity to proliferate.Blockade of the PD-1/PD-L1 pathway by the PD-L1-specific antibody partially restored cytokine production and cell proliferation.These data provide direct evidence that the PD-1/PD-L1 pathway is involved in CD81 T-cell dysfunction in NSCLC patients.Moreover,blocking this pathway provides a potential therapy target in lung cancer. | Yan Zhang Shengdong Huang Dejun Gong Yanghua Qin Qian Shen | 2010 | Cellular & Molecular Immunology2010，7，5： | 48 |
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