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IL-33 induces immunosuppressive neutrophils via a type 2 innate lymphoid cell/il-13/STAT6 axis and protects the liver against injury in LCMV infection-induced viral hepatitis

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Cellular & Molecular Immunology 2019年第2期16卷 126-137页

作者： Yuejin Liang Panpan Yi Denley Ming Kee Yuan Zuliang Jie Zakari Kwota Lynn Soong Yingzi Cong Jiaren Sun Department of Microbiology and Immunology University of Texas Medical BranchGalvestonTX 77555-1070USA Department of Infectious Diseases Key Laboratory of Viral Hepatitis of HunanXiangya HospitalCentral South UniversityChangsha 410008China Pathology and Institute for Human Infections and Immunity University of Texas Medical BranchGalvestonTX 77555-1070USA

Viral hepatitis is still a public health problem affecting several million people around the world.Neutrophils are polymorphonuclear cells that have a critical role in antibacterial infection.However,the role of neutrophils in viral infection is not fully understood.By using a mouse model of lymphocytic choriomeningitis virus infection-induced viral hepatitis,we observed increased neutrophil recruitment in the liver accompanied by enhanced CD8+T-cell responses.Liver neutrophils expressed high levels of immunomodulatory cytokines,such as C-X-C chemokine ligand 2,arginase-1,inducible nitric oxide synthase and interleukin(il)-10,demonstrating immunosuppressive properties.Depletion of neutrophils in vivo by a neutralizing antibody resulted in the exacerbation of liver injury and the promotion of T-cell responses at the immune contraction stage.IL-33 significantly induced neutrophil recruitment in the liver and attenuated liver injury by limiting effector T-cell accumulation.Mechanistically,we found that IL-33 promoted the expression of arginase-1 in neutrophils through the type 2 innate lymphoid cell(ilC2)-derived il-13.Additionally,il-13 increased the inhibitory effect of neutrophils on CD8+T-cell proliferation in vitro,partially through arginase-1.Finally,we found that il-13 induced arginase-1 expression,depending on signal transducer and activator of transcription factor 6(STAT6)signaling.Therefore,IL-33 induced immunosuppressive neutrophils via an ilC2/il-13/STAT6 axis.Collectively,our findings shed new light on the mechanisms associated with IL-33-triggered neutrophils in the liver and suggest potential targets for therapeutic investigation in viral hepatitis.

关键词： IL-33 ilC2 neutrophils viral infection liver

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The soluble glycoprotein NMB(GPNMB)produced by macrophages induces cancer sternness and metastasis via CD44 and IL-33

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Cellular & Molecular Immunology 2021年第3期18卷 711-722页

作者： M.Liguori E.Digifico A.Vacchini R.Avigni F.S.Colombo E.M.Borroni F.M.Farina S.Milanesi A.Castagna L.Mannarino I.Craparotta S.Marchini E.Erba N.Panini M.Tamborini V.Rimoldi P.Allavena C.Belgiovine IRCCS Humanitas Clinical and Research Center Via Manzoni 5620089 RozzanoMlItaly Department of Biomedical Sciences Humanitas Universityvia Rita Levi Montalcini 420089 Pieve EmanueleItaly Department of Medical Biotechnologies and Translational Medicine Universita degli Studi di MilanoVia Fratelli Cervi20090 SegrateItaly Department of Oncology Mario Negri Institute for Pharmacological Research IRCCS20156 MilanItaly

In cancer,myeloid cells have tumor-supporting roles.We reported that the protein GPNMB(glycoprotein nonmetastatic B)was profoundly upregulated in macrophages interacting with tumor cells.Here,using mouse tumor models,we show that macrophage-derived soluble GPNMB increases tumor growth and metastasis in Gpnmb-mutant mice(DBA/2J).GPNMB triggers in the cancer cells the formation of self-renewing spheroids,which are characterized by the expression of cancer stem cell markers,prolonged cell survival and increased tumor-forming ability.Through the CD44 receptor,GPNMB mechanistically activates tumor cells to express the cytokine IL-33 and its receptor UR1L. We also determined that recombinant IL-33 binding to il-1R1L is sufficient to induce tumor spheroid formation with features of cancer stem cells.Overall,our results reveal a new paracrine axis,GPNMB and IL-33,which is activated during the cross talk of macrophages with tumor cells and eventually promotes cancer cell survival,the expansion of cancer stem cells and the acquisition of a metastatic phenotype.

关键词： cancer stem cells GPNMB IL-33 metastasis tumor associated macrophages

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Exosomes from bone marrow mesenchymal stem cells are a potential treatment for ischemic stroke

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Neural Regeneration Research 2023年第10期18卷 2246-2251页

作者： Chang Liu Tian-Hui Yang Hong-Dan Li Gong-Zhe Li Jia Liang Peng Wang Liaoning Provincial Key Laboratory of Neurodegenerative Diseases and Department of Neurobiology Jinzhou Medical UniversityJinzhouLiaoning ProvinceChina Institute of Life Science Jinzhou Medical UniversityJinzhouLiaoning ProvinceChina College of Pharmacy Jinzhou Medical UniversityJinzhouLiaoning ProvinceChina

Exosomes derived from human bone marrow mesenchymal stem cells(MSC-Exo)are characterized by easy expansion and storage,low risk of tumor formation,low immunogenicity,and anti-inflammatory effects.The therapeutic effects of MSC-Exo on ischemic stroke have been widely explored.However,the underlying mechanism remains unclear.In this study,we established a mouse model of ischemic brain injury induced by occlusion of the middle cerebral artery using the thread bolt method and injected MSC-Exo into the tail vein.We found that administration of MSC-Exo reduced the volume of cerebral infarction in the ischemic brain injury mouse model,increased the levels of interleukin-33(IL-33)and suppression of tumorigenicity 2 receptor(ST2)in the penumbra of cerebral infarction,and improved neurological function.In vitro results showed that astrocyte-conditioned medium of cells deprived of both oxygen and glucose,to simulate ischemia conditions,combined with MSC-Exo increased the survival rate of primary cortical neurons.However,after transfection by IL-33 siRNA or ST2 siRNA,the survival rate of primary cortical neurons was markedly decreased.These results indicated that MSC-Exo inhibited neuronal death induced by oxygen and glucose deprivation through the IL-33/ST2 signaling pathway in astrocytes.These findings suggest that MSC-Exo may reduce ischemia-induced brain injury through regulating the IL-33/ST2 signaling pathway.Therefore,MSC-Exo may be a potential therapeutic method for ischemic stroke.

关键词： astrocytes bone marrow mesenchymal stem cells brain injury exosome IL-33 inflammation ischemic stroke neurological function neuron ST2

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IL-33稳定沉默后通过削弱AKT磷酸化抑制间充质干细胞增殖

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中国免疫学杂志 2022年第7期38卷 783-788页

作者：高建华叶小磊郭莹叶方义湖(指导) 江西医学高等专科学校基础医学部上饶334000 西华师范大学生命科学学院南充637000

目的:通过慢病毒载体沉默IL-33在间充质干细胞(MSCs)中的表达,探讨IL-33基因沉默后对MSCs增殖、凋亡的影响及其作用机制。方法:通过构建IL-33基因的shRNA慢病毒载体转染MSCs;应用RT-PCR及免疫印迹方法检测IL-33在MSCs中的表达情况及il-3... 详细信息

目的:通过慢病毒载体沉默IL-33在间充质干细胞(MSCs)中的表达,探讨IL-33基因沉默后对MSCs增殖、凋亡的影响及其作用机制。方法:通过构建IL-33基因的shRNA慢病毒载体转染MSCs;应用RT-PCR及免疫印迹方法检测IL-33在MSCs中的表达情况及IL-33基因的沉默效果;通过Annexin V/PI流式细胞术检测细胞凋亡情况,进而检测IL-33基因沉默后对MSCs增殖、凋亡的影响,并通过免疫印迹检测AKT磷酸化水平。结果:细胞转染及免疫印迹实验表明IL-33 shRNA慢病毒载体构建成功,并干扰了IL-33在MSCs中的表达;稳定沉默IL-33基因后,MTT细胞生长实验表明MSCs增殖能力减弱(PIL-33基因沉默后可提高MSCs对外界凋亡诱导物的敏感性,且引起细胞survivin基因表达的下调。结论:IL-33基因可能与MSCs增殖和抗凋亡有关,进而参与MSCs的发育和存活,IL-33稳定沉默后通过削弱AKT磷酸化可抑制MSCs增殖。

关键词：间充质干细胞 IL-33 细胞转染凋亡

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IL-33缺陷调节小鼠抗弓形虫感染的CD8^(+)T细胞应答

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中国人兽共患病学报 2023年第6期39卷 550-555页

作者：何小丽陈杏婷吴林青潘垚陈舒玲韩艳非陈义忠章涛福建医科大学基础医学院福州350122 福建医科大学附属第一医院福州350005 上海市医疗器械化妆品审评核查中心上海200020

目的探讨IL-33缺陷(IL-33^(-/-))对弓形虫感染小鼠的炎症反应和CD8^(+)T细胞功能的影响。方法C57BL/6野生型(Wild-type,WT)和IL-33^(-/-)小鼠分别设感染组和对照组,建立弓形虫感染模型,记录小鼠死亡时间,绘制生存曲线;分别取感染后48 h... 详细信息

目的探讨IL-33缺陷(IL-33^(-/-))对弓形虫感染小鼠的炎症反应和CD8^(+)T细胞功能的影响。方法C57BL/6野生型(Wild-type,WT)和IL-33^(-/-)小鼠分别设感染组和对照组,建立弓形虫感染模型,记录小鼠死亡时间,绘制生存曲线;分别取感染后48 h、96 h各组小鼠外周血及肝、脾组织,HE染色观察组织病理变化;微量样本多指标流式蛋白定量技术(cytometric bead array,CBA)及ELISA检测血浆炎症因子(il-12P70、TNF-α、IFN-γ、MCP-1、il-6及il-4)水平;qPCR检测小鼠脾细胞中弓形虫速殖子表面抗原-1(SAG-1)的mRNA水平;流式细胞术分析脾脏CD8^(+)T细胞穿孔素、颗粒酶和IFN-γ水平。结果与WT感染组小鼠比较,96 h时IL-33^(-/-)感染组小鼠脾脏SAG-1 mRNA表达降低(F=13.96,PIL-33^(-/-)感染组血浆il-4浓度升高较高(F=328.32,PIL-33^(-/-)感染组小鼠脾脏CD8^(+)T细胞穿孔素(F=574.20,PIL-33抑制脾脏CD8^(+)T细胞应答,促进全身炎症反应。

关键词： IL-33 弓形虫感染 T细胞炎症反应小鼠

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炎症因子IL-33通过mTOR/Akt信号通路调节肥大细胞反应抑制萎缩性胃炎

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免疫学杂志 2022年第4期38卷 324-331页

作者：杨敬端何明吴品南阳医学高等专科学校第一附属医院消化内科 473000

目的探究IL-33、肥大细胞和TNF-α在幽门螺杆菌诱导的萎缩性胃炎中的相互作用并初步探究其涉及的信号通路。方法通过RT-qPCR检测IL-33和TNF-α的mRNA表达水平;Western blot及ELISA检测IL-33和TNF-α的蛋白表达水平;通过免疫组织化学染... 详细信息

目的探究IL-33、肥大细胞和TNF-α在幽门螺杆菌诱导的萎缩性胃炎中的相互作用并初步探究其涉及的信号通路。方法通过RT-qPCR检测IL-33和TNF-α的mRNA表达水平;Western blot及ELISA检测IL-33和TNF-α的蛋白表达水平;通过免疫组织化学染色人胃炎组织检测肥大细胞浸润;免疫荧光染色证明IL-33与其受体ST2和胰蛋白酶的表达及其在幽门螺杆菌感染的胃黏膜肥大细胞上共定位。最后通过Western blot检测mTOR抑制剂Rapamycin和AKT抑制剂MK2206处理组IL-33、p-mTOR/mTOR和p-AKT/AKT蛋白的表达。结果RT-qPCR、ELISA及Western blot检测结果表明,在幽门螺杆菌感染患者和小鼠中,IL-33的mRNA和蛋白表达水平都显著升高;HE染色和ELISA检测结果表明,IL-33的中和显著降低了胃炎症,减少了TNF-α的产生,而注射IL-33能显著增加胃炎症和TNF-α的产生。免疫组织化学和免疫荧光染色检测结果表明,在幽门螺杆菌感染的胃黏膜中有肥大细胞浸润且比对照组数量显著增加,IL-33与肥大细胞表面受体ST2共定位。最后,Western blot实验结果显示,mTOR和AKT抑制剂,可以逆转幽门螺杆菌感染引起的mTOR/AKT信号通路激活。结论幽门螺旋杆菌诱导胃黏膜组织表达IL-33,它可以通过与肥大细胞表面IL-33受体ST2相互作用诱导肥大细胞活化和促炎介质TNF-α的产生。因此,我们的研究结果将幽门螺杆菌感染与肥大细胞活化联系起来。

关键词： IL-33 肥大细胞萎缩性胃炎幽门螺杆菌 mTOR/Akt

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MHD患者院内感染的病原学特征及SII、PLR、IL-33检测对感染的预测

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中国病原生物学杂志 2022年第9期17卷 1090-1094页

作者：杨荆樊文星毕丹青昆明医科大学第一附属医院肾脏内科云南昆明650032

目的探讨维持性血液透析(MHD)患者院内感染病原菌类型及其特征,并对全身免疫炎症指数(SII)、血小板/淋巴细胞比值(PLR)及白细胞介素-33(IL-33)水平预测其发生院内感染的价值进行分析。方法2018年6月-2021年6月于我院治疗的823例MHD患者... 详细信息

目的探讨维持性血液透析(MHD)患者院内感染病原菌类型及其特征,并对全身免疫炎症指数(SII)、血小板/淋巴细胞比值(PLR)及白细胞介素-33(IL-33)水平预测其发生院内感染的价值进行分析。方法2018年6月-2021年6月于我院治疗的823例MHD患者作为研究对象,根据其住院治疗是否发生院内感染将其分为感染组(n=170)和非感染组(n=653)。分析其感染病原菌的分布特点,并收集临床资料,采用单因素和多因素分析与院内感染相关的危险因素。检测两组患者SII、PLR及IL-33水平变化,并通过受试者工作曲线(ROC)分析以上因子对患者院内感染的预测价值。结果823例MHD患者中,170例发生院内感染,感染率为20.66%(170/823),其中以呼吸道感染为主(感染率为40.00%),其次是泌尿道、静脉导管及消化道感染,感染率分别为23.53%、20.00%、10.00%。170例MHD患者发生院内感染的主要致病菌为革兰阴性菌103株(占60.59%),其中以大肠埃希菌(35株,20.59%)、铜绿假单胞菌(24株,14.12%)及肺炎克雷伯菌(18株,10.59)为主;革兰阴性菌48株(占28.24%),以金黄色葡萄球菌(17株,10.00%)为主;真菌感染主要致病菌为白假丝酵母菌(10株,5.88%)。单因素分析结果显示,患者的年龄、首次透析住院时间、合并PEW、血红蛋白水平、血浆白蛋白水平、SII、PLR及IL-33水平等因素与其发生院内感染存在显著相关性(χ^(2)=63.955,t=5.707,2.036,29.929,8.814,42.486,6.928,PIL-33等水平升高均是导致MHD患者发生院内感染的独立危险因素(均P33水平预测MHD患者发生院内感染的AUC分别为0.744(95%CI:0.595~0.893)、0.737(95%CI:0.580~0.894)及0.723(95%CI:0.576~0.869)(PIL-33水平均为MHD患者发生院内感染的危险因素。分析院内感染并病原菌分布特点,并检测SII、PLR及IL-33水平对预防MHD发生院内感染具有积极意义。

关键词： MHD患者院内感染病原学特征 SII PLR IL-33

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Potential role of the IL-33/ST2 axis in celiac disease

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Cellular & Molecular Immunology 2017年第3期14卷 285-292页

作者： Lopez-Casado MA Lorite P Palomeque T Torres MI Department of Pediatrics Gastroenterology Hospital Virgen de las Nieves Granada Spain Department of Experimental Biology University of Jaen Jaen Spain

The IL-33/ST2 axis has been implicated in the pathogenesis of several tissue-specific autoimmune diseases. Celiac disease （CD） is the only autoimmune disease in which both the major genetic factors （HLA-DQ2/DQ8） and etiologic ones （dietary gluten） for susceptibility are known. We have measured serum levels and determined intestinal tissue expression of IL-33 and its receptor soluble ST2 in patients with CD to investigate their association with disease activity. Serum and tissue levels of both IL-33 and sST2 were significantly higher in patients with CD compared with those in control patients without CD. We show that toxic peptides extracted from barley and wheat gliadin significantly stimulate the production of IL-33 and ST2 in cultured peripheral blood mononuclear cell from celiac patients, strongly implicating the IL-33/ST2 axis in the pathogenesis of CD. The higher levels of IL-33 and its receptor ST2 in tissue and serum reflect an active inflammatory state and may represent a potential biomarker for disease activity. A better understanding of IL-33/ ST2 release, mode of action, and regulation will be crucial to develop therapeutics that target the IL-33/ST2 pathway to treat CD.

关键词： celiac disease gluten peptides IL-33 ST2

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Bach2对Th2细胞内IL-33生物学功能的影响

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中国免疫学杂志 2022年第10期38卷 1153-1157页

作者：刘果于凌昱马腾飞刘锋四川大学华西医院耳鼻咽喉头颈外科成都610041

目的:探讨Bach2与Th2细胞内IL-33生物学功能的关系。方法:构建Bach2基因的条件敲除小鼠(Bach2-CKO小鼠),将Bach2-CKO小鼠与正常小鼠分为两组,IL-33经鼻诱导Th2型免疫应答,对比分析两组小鼠肺部炎症情况;从小鼠脾脏中分离na?ve CD4^(+)T... 详细信息

目的:探讨Bach2与Th2细胞内IL-33生物学功能的关系。方法:构建Bach2基因的条件敲除小鼠(Bach2-CKO小鼠),将Bach2-CKO小鼠与正常小鼠分为两组,IL-33经鼻诱导Th2型免疫应答,对比分析两组小鼠肺部炎症情况;从小鼠脾脏中分离na?ve CD4^(+)T细胞并诱导分化为Th2细胞;下调(或上调)细胞内Bach2表达后给予IL-33刺激,检测Th2型细胞因子表达。结果:与正常小鼠相比,IL-33显著增加Bach2-CKO小鼠肺组织内炎症细胞浸润、黏液腺分泌以及il-4、il-5和il-13mRNA表达;与正常Th2细胞相比,IL-33更加显著地促进Bach2-/-Th2细胞il-5和il-13表达(PIL-33相关il-5和il-13表达(PIL-33/ST2信号通路调控,可有效抑制该细胞内IL-33的生物学功能。

关键词： Bach2 IL-33 Th2细胞 Th2型炎症反应信号通路

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HMGB1, il-1α, IL-33 and S100 proteins： dual-function alarmins

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Cellular & Molecular Immunology 2017年第1期14卷 43-64页

作者： Damien Bertheloot Eicke Latz Institute of Innate Immunity University Hospitals University of Bonn 53127 Bonn Germany German Center for Neurodegenerative Diseases (DZNE) 53117 Bonn Germany Department of Infectious Diseases and Immunology University of Massachusetts Medical School Worcester MA 01605 USA

Our immune system is based on the close collaboration of the innate and adaptive immune systems for the rapid detection of any threats to the host. Recognition of pathogen-derived molecules is entrusted to specific germline- encoded signaling receptors. The same receptors have now also emerged as efficient detectors of misplaced or altered self-molecules that signal tissue damage and cell death following, for example, disruption of the blood supply and subsequent hypoxia. Many types of endogenous molecules have been shown to provoke such sterile inflammatory states when released from dying cells. However, a group of proteins referred to as alarmins have both intracellular and extracellular functions which have been the subject of intense research. Indeed, alarmins can either exert beneficial cell housekeeping functions, leading to tissue repair, or provoke deleterious uncontrolled inflammation. This group of proteins includes the high-mobility group box 1 protein （HMGB1）, interleukin （il）-1α, IL-33 and the Ca^2＋-binding S100 proteins. These dual-function proteins share conserved regulatory mechanisms, such as secretory routes, post-translational modifications and enzymatic processing, that govern their extracellular functions in time and space. Release of alarmins from mesenchymal cells is a highly relevant mechanism by which immune cells can be alerted of tissue damage, and alarmins play a key role in the development of acute or chronic inflammatory diseases and in cancer development.

关键词： alarmin HMGB1 il-1α IL-33 inflammation S100 proteins

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