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An unbalanced PD-L1/CD86 ratio in CD14^＋＋CD16^＋ monocytes is correlated with HCV viremia during chronic HCV infection

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Cellular & Molecular Immunology 2014年第3期11卷 294-304页

作者： Jiajia Zheng Hua Liang Chunhui Xu Qiang Xu Ting Zhang Tao Shen Fengmin LU Department of Microbiology Peking University Health Science Center Beijing China Department of Laboratory Medicine Peking University Third Hospital Beijing China State Key Laboratory for infectious Disease Prevention and Control National Center for AIDS/STD Control and Prevention China CDC Beijing China Center of Infectious Diseases Peking University Beijing China These authors contributed equally to this work

Circulating monocyte subsets with distinct functions play important roles in hepatitis C virus （HCV） infection. However, the mechanisms have not been well studied. In this study, we analyzed the distributions and phenotypic characteristics of three circulating monocyte subsets--CD14^＋＋CD16^-, CD14^＋＋CD16^＋ and CD14^＋＋mCD16^——in chronic HCV-infected patients, HCV spontaneous resolvers and healthy controls, and we evaluated the possible link between HCV viremia and disease progression. Our results indicated that the frequency of the CD 14^＋＋CD 16^＋ monocyte subset was decreased, and negatively correlated with HCV RNA and core antigen levels during chronic HCV infection. PD-L1 expression and the PD-L1/CD86 ratio in CD14^＋＋CD16^＋ monocytes were higher during chronic HCV infection than in spontaneous HCV resolvers and healthy controls. The PD-L1/CD86 ratio positively correlated with HCV viral load and core antigen levels. Finally, PD-L1 was significantly increased, while cytokine secretions were dramatically decreased upon Toll-like receptor （TLR） ligand binding and HCV JFH-lstimulation. These findings indicates the compromised immune status of the CD14^＋＋CD16^＋ monocytes during chronic HCV infection and provides new insights into the specific role of the CD14^＋＋CD16^＋ monocytes and their significance in chronic HCV infection.

关键词： core antigen hepatitis C virus monocytes PD-L1/CD86 viral load

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Insoluble β-glucan from the cell wall of Candida albicans induces immune responses of human THP-1 monocytes through Dectin-1

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Chinese Medical Journal 2009年第5期122卷 496-501页

作者： LI Min LIU Ze-hu CHEN Qing ZHOU Wu-qing YU Mei-wen Lü Gui-xia LU Xue-lian SHEN Yong-nian LIU Wei-da WU Shao-xi Department of Medical Mycology Institute of Dermatology Chinese Academy of Medical Science & Peking Union Medical College Nanjing 210042 China Developmental Therapeutics Program Barbara Ann Karmanos Cancer Institute Departments of Pediatrics Wayne State University School of Medicine Detroit MI 48201 USA (Chen Q)

Background β-glucan is the major structure component of Candida albicans （C. albicans） cell wall. It has been demonstrated that Dectin-1 as the principal C-type lectin pattern-recognition receptor （PRR） can recognize fungal β-glucan and induce immune responses. In this study, we sought to clarify whether insoluble β-glucan from the cell wall of C. albicans （CalG） could induce immune responses in human THP-1 monocytes （a human acute monocytic leukemia cell line） and to determine the underlying mechanisms. Methods Human THP-1 monocytes were challenged with CalG in vitro. The mRNA expression of Dectin-1, Toll-like receptors （TLR2）, proinflammatory cytokine （TNF-a） and chemokine （IL-8） was assayed by real-time reverse transcription polymerase chain reaction （RT-PCR）. The secretion of TNF-a and IL-8 were measured by enzyme-linked immunosorbent assay （ELISA）. H2O2 release was determined by microplate fluorescent assay. Western blotting was used to analyze IKB-a phosphorylation and degradation. Results Exposure of THP-1 monocytes to CalG led to increased gene expression and secretion of TNF-a and IL-8. CalG induced H2O2 release in a time-dependent manner. CalG hydrolyzed with zymolyase failed to induce gene expression and secretion of TNF-a, IL-8 and H2O2 release. CalG up-regulated the mRNA of Dectin-1, whereas the mRNA level of TLR2 was not altered. THP-1 monocytes challenged with CalG resulted in the activation of NF-KB in a time-dependent manner. Dectin-1 inhibitor laminarin blocked the CalG-induced production of TNF-a and H2O2 in THP-1 monocytes, but no such effect was observed in pretreatment with anti-TLR2 neutralizing antibody and the LPS inhibitor （polymyxin B）. Conclusion CalG may play a role in activation of immune responses in human THP-1 cells throuah Dectin-1, not TLR2.

关键词： Candida albicans monocytes insoluble β-glucan Dectin-1 cytokines hydrogen peroxide

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TREM-1 multimerization is essential for its activation on monocytes and neutrophils

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Cellular & Molecular Immunology 2019年第5期16卷 460-472页

作者： Kevin Carrasco Amir Boufenzer Lucie Jolly Helene Le Cordier Guanbo Wang Albert JR Heck Adelheid Cerwenka Emilie Vinolo Alexis Nazabal Alexandre Kriznik Pierre Launay Sebastien Gibot Marc Derive INOTREM Vandœuvre-les-NancyFrance UMR-S 1116 Defaillance cardiovasculaire aigue et chroniqueVandœuvre-les-NancyFrance UMR7365 Ingénierie Moléculaire et Physiopathologie Articulaire(IMoPA)CNRS-Universitéde LorraineVandœuvre-les-NancyFrance Biomolecular Mass Spectrometry and Proteomics Bijvoet Center for Biomolecular Research and Utrecht Institute for Pharmaceutical Sciences and Netherlands Proteomics CenterUtrecht UniversityUtrechtThe Netherlands Innate Immunity German Cancer Research Center(DKFZ)HeidelbergGermany CovalX ZurichSwitzerland Service Commun de Biophysique Interactions Moléculaires(SCBIM) FR3209Biopole de l’Universitede LorraineVandœuvre-les-NancyFrance Inatherys Evry CedexFrance

The triggering receptor expressed on myeloid cells-1(TREM-1)is a receptor expressed on innate immune *** promoting the amplification of inflammatory signals that are initially triggered by Toll-like receptors(TLRs),TREM-1 has been characterized as a major player in the pathophysiology of acute and chronic inflammatory diseases,such as septic shock,myocardial infarction,atherosclerosis,and inflammatory bowel ***,the molecular events leading to the activation of TREM-1 in innate immune cells remain ***,we show that TREM-1 is activated by multimerization and that the levels of intracellular Ca 2+release,reactive oxygen species,and cytokine production correlate with the degree of TREM-1 ***-1 activation on primary human monocytes by LPS required a two-step process consisting of upregulation followed by clustering of TREM-1 at the cell surface,in contrast to primary human neutrophils,where LPS induced a rapid cell membrane reorganization of TREM-1,which confirmed that TREM-1 is regulated differently in primary human neutrophils and *** addition,we show that the ectodomain of TREM-1 is able to homooligomerize in a concentration-dependent manner,which suggests that the clustering of TREM-1 on the membrane promotes its *** further show that the adapter protein DAP12 stabilizes TREM-1 surface expression and ***-1 multimerization at the cell surface is also mediated by its endogenous ligand,a conclusion supported by the ability of the TREM-1 inhibitor LR12 to limit TREM-1 *** results provide evidence for ligand-induced,receptor-mediated dimerization of ***,our findings uncover the mechanisms necessary for TREM-1 activation in monocytes and neutrophils.

关键词： TREM-1 multimerization activation monocytes neutrophils

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The IRAK-ERK-p67phox-Nox-2 axis mediates TLR4, 2-induced ROS production for IL-lp transcription and processing in monocytes

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Cellular & Molecular Immunology 2016年第6期13卷 747-763页

作者： Ankita Singh Vishal Singh Rajiv L. Tiwari Tulika Chandra Ashutosh Kumar Madhu Dikshit Manoj K. Barthwal Pharmacology Division CSIR-Central Drug Research Institute B.S. 10/1 Sector 10 Sitapur Road Jankipuram Extension Lucknow 226031 Uttar Pradesh India Department of Transfusion Medicine and Blood Bank King George's Medical University Lucknow Uttar Pradesh India Department of Pathology King George's Medical University Lucknow Uttar Pradesh India

In monocytic cells, Toll-like receptor 4 （TLR4）- and TLR2-induced reactive oxygen species （ROS） cause oxidative stress and inflammatory response; however, the mechanism is not well understood. The present study investigated the role of interleukin-1 receptor-associated kinase （IRAK）, extracellular signal-regulated kinase （ERK）, p67phox and Nox-2 in TLR4- and TLR2-induced ROS generation during interleukin-1 beta （IL-1β） transcription, processing, and secretion. An IRAK1/4 inhibitor, U0126, PD98059, an NADPH oxidase inhibitor （diphenyleneiodonium （DPI））, and a free radical scavenger （N-acetyl cysteine （NAC））-attenuated TLR4 （lipopolysaccharide （LPS））- and TLR2 （Pam3csk4）-induced ROS generation and IL-1β production in THP-1 and primary human monocytes. An IRAK1/4 inhibitor and siRNA-attenuated LPS- and Pam3csk4-induced ERK-IRAK1 association and ERK phosphorylation and activity. LPS and Pam3csk4 also induced IRAK1/4-, ERK- and ROS-dependent activation of activator protein-1 （AP-1）, IL-1β transcription, and IL-1β processing because significant inhibition in AP-1 activity, IL-lp transcription, Pro- and mature IL-p expression, and caspase-1 activity was observed with PD98059, U0126, DPI, NAC, an IRAK1/4 inhibitor, tanshinone Ila, and IRAK1 siRNA treatment. IRAK-dependent ERK-p67phox interaction, p67phox translocation, and p67phox-Nox-2 interaction were observed. Nox-2 siRNA significantly reduced secreted IL-lp, IL-1β transcript, pro- and mature IL-1β expression, and caspase-1 activity indicating a role for Nox-2 in LPS- and Pam3csk4-induced IL-1β production, transcription, and processing. In the present study, we demonstrate that the TLR4- and TLR2-induced IRAK-ERK pathway cross-talks with p67phox-Nox-2 for ROS generation, thus regulating IL-1β transcription and orocessin; in monocvtic cells.

关键词： IL-1β IRAK monocytes ROS TLR

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Chemokine RANTES is upregulated in monocytes from patients with hyperhomocysteinemia

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Acta Pharmacologica Sinica 2005年第11期26卷 1317-1321页

作者： Wei SUN~(2,5), Guang WANG~(3,5), Zhen-min ZHANG~4, Xiao-kun ZENG~2, Xian WANG~(2,4,6) ~2 Institute of Vascular Medicine ~3 Department of Gerontology, Peking University Third Hospital ~4 Department of Physiology and Pathophysiology, Key Laboratory of Molecular Cardiovascular Science, Ministry of Education, Basic Medical College, Peking University, Beijing 100083, China Institute of Vascular Medicine Peking University Third Hospital Beijing China Department of Gerontology Peking University Third Hospital Beijing China Department of Physiology and Pathophysiology Key Laboratory of Molecular Cardiovascular Science Ministry of Education Basic Medical College Peking University Beijing China

Aim: To investigate the changes in plasma level of the chemokine RANTES (regulated upon activation, normal T cells expressed and secreted) and the responsiveness of lipopolysaccharide (LPS)-induced RANTES secretion from monocytes in patients with hyperhomocysteinemia (HHcy). Methods: The plasma levels of homocysteine (Hcy), folate, and RANTES were measured in 38 control patients with normal Hcy levels and 40 patients with HHcy and the mRNA synthesis of RANTES in isolated human monocytes was determined by RNase protection assays. Results: The plasma level of RANTES was elevated in HHcy patients compared with controls (median 5.3 vs 3.5 ng/mL, Pmonocytes of HHcy patients was also increased significantly. In addition, Hcy directly increased the mRNA level of RANTES in isolated normal human monocytes in a time- and dose-dependent manner. Conclusion: Upregulated RANTES from monocytes in HHcy patients may be involved in the atherogenesis of HHcy-induced atherosclerosis.

关键词： homocysteine monocytes RANTES folic acid atherosclerosis humans

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Essential role of monocytes and macrophages in the progression of acute pancreatitis

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World Journal of Gastroenterology 2010年第32期16卷 3995-4002页

作者： Pratima Shrivastava Madhav Bhatia Department of Pharmacology National University of SingaporeSingapore 117597Singapore Department of Pathology University of OtagoChristchurch 8140New Zealand

Acute pancreatitis(AP) is an inflammatory condition of the pancreas caused by an imbalance in factors involved in maintaining cellular *** events in AP occur within acinar cells accompanied by other principal contributors to the inflammatory response *** endothelial cells,immunocytes(granulocytes,monocytes/macrophages,lymphocytes) and ***/macrophages are important inflammatory mediators,involved in the pathophysiology of AP,known to reside in the peritoneal cavity(in the vicinity of the pancreas) and in peripancreatic *** studies suggested that impaired clearance of injured acini by macrophages is associated with an altered cytokine reaction which may constitute a basis for progression of *** review focuses on the role of monocytes/macrophages in progression of AP and discusses f indings on the inflammatory process involved.

关键词： Acute pancreatitis monocytes Peritoneal macrophages Alveolar macrophages Kupffer cells

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Genistein inhibits human TNF-α-induced porcine endothelial cell adhesiveness for human monocytes and natural killer cells

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Chinese Science Bulletin 2002年第6期47卷 470-475页

作者： Xiaofeng Zhang Yan Gu Zhimin Feng Liqin Ban Meifu Feng National Laboratory of Biomembrane and Membrane Biotechnology Institute of Zoology Chinese Academy of Sciences Beijing China

Cellular immune response is a major barrier to xenotransplantation. Human tumor necrosis factor-α (hTNF-α) possesses cross-species activity and directly amplifies the immune rejection via the upregulation of adhesion molecules on porcine endothelium. We investigated the role of protein tyrosine phosphorylation in the induction of expression of E-selectin and vascular cell adhesion molecule-1 (VCAM-1), and the augmentation of adhesion of human peripheral blood monocytes (PBMo) and natural killer cells (PBNK), after rhTNF-α-stimulation of porcine aortic endo-thelial cells (PAEC) in vitro. rhTNF-α-increased adhesiveness of PAEC for both PBMo and PBNK was dose-dependently reduced by pretreatment of PAEC with the selective protein tyrosine kinase (PTK) inhibitor genistein. The inhibitory effect occurred at the early time of PAEC activation triggered by rhTNF-α, and was completely reversible. PTK activity assay indicated that genistein also suppressed rhTNF-α stimulated activation of protein tyrosine

关键词： genistein human tumor necrosis factor-α (hTNF-α) porcine aortic endothclial cells (PAEC) human peripheral blood monocytes (PBMo) human peripheral blood natural killer cells (PBNK) cell adhesion.

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Interindividual Heterogeneity of Hypoxic Response of Vascular Endothelial Growth Factor and Intercellular Adhesive Molecule-1 in monocytes from Diabetic Patients

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Chinese Medical Journal 2016年第23期129卷 2882-2884页

作者： Zhi-Kun Yang Zhuo-Zai Xu Xiao Zhang Fei Gao Wei-Hong Yu Department of Ophthalmology Peking Union Medical College Hospital Chinese Academy of Medical Sciences Beijing 100730 China Department of Ophthalmology Beijing Chaoyang Hospital Capital Medical University Beijing 100020 China

Diabetic retinopathy （DR） is one of the leading causes of legal blindness worldwide. The development and progression of DR are related to a variety of factors, such as the age of onset, the duration and type of diab... 详细信息

关键词： Diabetes Diabetic Retinopathy Hypoxia In vitro Intercellular Adhesive Molecule-1 monocytes Vascular Endothelial Growth Factor

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Asialoglycoprotein receptor 1 gene expression in peripheral blood monocytes associates with serum total cholesterol and low-density lipoprotein cholesterol levels

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Chinese Medical Journal 2020年第12期133卷 1505-1506页

作者： Xiang Zhao Bin Tang Zhi-Hua Shi Zi-Wei Deng Ye Deng Li-Ming Tan Shi-Long Jiang Yuan-Lu Shu Cheng-Feng Qiu Department of General Practice The First People’s Hospital of HuaihuaUniversity of South ChinaHuaihuaHunan 418000China Department of Evidence-based Medicine and Clinical Center The First People’s Hospital of HuaihuaUniversity of South ChinaHuaihuaHunan 418000China Department of Pharmacology The First People’s Hospital of HuaihuaUniversity of South ChinaHuaihuaHunan 418000China Department of Pharmacology The Second People’s Hospital of Huaihua CityHuaihuaHunan 418000China Department of Clinical Pharmacology Xiangya Hospital Central South UniversityChangshaHunan 410008China

To the Editor:Asialoglycoprotein receptor 1(ASGR1)is the major subunit of ASGR,it is predominantly expressed by liver parenchymal cells and relatively lower expression was found in peripheral blood monocytes.[1]A genetic study recently revealed that ASGR1 haploinsufficiency resulted from loss-of-function(LOF)variants was strongly associated with the pronounced reductions in serum total cholesterol(TC)and low-density lipoprotein cholesterol(LDL-C)levels,[2,3]suggesting that ASGR1 may play a key role in cholesterol ***,the function of ASGR1 remains largely *** study was focused on the association of ASGR1 gene expression in monocytes and plasma cholesterol level.

关键词： cholesterol lipoprotein monocytes

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Dilazep and dipyridamole inhibit tissue factor expressionon monocytes induced by IgG from patientswith antiphospholipid syndrome

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Acta Pharmacologica Sinica 2004年第10期 126-131页

作者： Hong ZHOUDepartment of Clinical Laboratory and Hematology, Jiangsu University School of Medical Technology, Zhenjiang 212001, China

AIM: To investigate whether antiplatelet agents, dilazep and dipyridamole, inhibit tissue factor (TF) expression on monocytes induced by IgG from patients with antiphospholipid syndrome (APS). METHODS: Freshly isolated peripheral blood monocytes were allowed to adhere on plastic and then cultured in media containing patient or control antibodies and/or other agonists with or without dilazep or dipyridamole. The TF activity on monocytes was investigated by measuring factor VIIa-dependent generation of factor Xa, using a chromogenic substrate and the TF mRNA expression was examined by real-time PCR (TaqMan PCR). RESULTS: The TF activity on monocytes induced by APS IgG (250 mg/L) was inhibited by dilazep (0.15-150 μmol/L) and dipyridamole (0.2-200 μmol/L) in a dose-dependent fashion. But, the TF mRNA expression induced by APS IgG was not inhibited. Theophylline (500 μmol/L), an adenosine receptor antagonist, could counteract the inhibitory effect of dilazep and dipyridamole on TF activity. CONCLUSION: An

关键词： dilazep dipyridamole antiphospholipid syndrome monocytes thromboplastin

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