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Specific function and modulation of teleost monocytes/macrophages: polarization and phagocytosis 被引量:7
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作者 Xin-Jiang Lu Jiong Chen 《Zoological Research》 SCIE CAS CSCD 2019年第3期146-150,共5页
Macrophages exist in most tissues and play a variety of functions in vertebrates.Teleost fish species are found in most aquatic environments throughout the world and are quite diverse for a group of vertebrate animals... Macrophages exist in most tissues and play a variety of functions in vertebrates.Teleost fish species are found in most aquatic environments throughout the world and are quite diverse for a group of vertebrate animals.Due to whole genome duplication and en vironme ntal adaptati on,teleost monocytes/macrophages possess a variety of different functions and modulations compared with those of mammals.A deeper understanding of teleost monocytes/macrophages in the immune system will not only help develop teleost-specific methods of disease prevention but will also help improve our understanding of the various immune mechanisms in mammals.In this review,we summarize the differences in polarizati on and phagocytosis of teleost and mammalian macrophages to improve our understanding of the various immune mechanisms in vertebrates. 展开更多
关键词 TELEOST monocytes/macrophages PHAGOCYTOSIS CYTOKINE producti on Comparative IMMUNOLOGY
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Comparison of YKL-39 and CHIT-1 expression during macrophages differentiation and polarization
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作者 Michelino Di Rosa Daniele Tibullo +2 位作者 Michele Malaguarnera Michele Tuttobene Lucia Malaguarnera 《Modern Research in Inflammation》 2013年第4期82-89,共8页
The chitinase-like proteins YKL-39 (chitinase 3-like-2) and Chitortriosidase (CHIT-1) are members of the chitinases family. YKL-39 expression has been associated with osteoarthritis, whereas CHIT-1 activity is regarde... The chitinase-like proteins YKL-39 (chitinase 3-like-2) and Chitortriosidase (CHIT-1) are members of the chitinases family. YKL-39 expression has been associated with osteoarthritis, whereas CHIT-1 activity is regarded as a biochemical marker of macrophage activation. So far, the physiological or pathological role of YKL-39 in the inflammation is still poorly understood. We compared YKL-39 and CHIT-1 modulation during monocyte to macrophage transition and polarization. Gene expression analysis was investigated by real-time PCR from mRNA of human monocytes obtained from buffy coat of healthy volunteers, from mRNA of polarized macrophages to classically activated macrophages (or M1), obtained by interferon-γ and lipopolysaccharide exposure, and from mRNA of alternatively activated macrophages (or M2) obtained by interleukin-4 exposure. We demonstrated different variations of YKL-39 and CHIT-1 production during macrophages polarization. CHIT-1 levels gradually increase in the course of the time with a peak of expression between the fifth and the seventh day of culture. In contrast, YKL-39 expression was unaltered in the diverse stage of HMMs differentiation, but increased significantly in M1 polarized macrophages and reverted to base levels in M2 polarized macrophages. These findings indicated that the function of YKL-39 is much more restricted and selective than that exerted by CHIT-1. 展开更多
关键词 YKL-39 CHITOTRIOSIDASE Human monocyte/macrophages Classically ACTIVATED macrophages Alternatively ACTIVATED macrophages
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Celastrol inhibits inflammatory factors expression in glioblastoma
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作者 Na Qin Shu-Xian Yang +1 位作者 Shi-Man Gao Ting Zhu 《Traditional Medicine Research》 2024年第6期1-11,共11页
Background:Glioblastoma is one of the most common primary intracranial tumors of the central nervous system in adults.Although chemotherapy is an important component of glioblastoma treatment,its effectiveness remains... Background:Glioblastoma is one of the most common primary intracranial tumors of the central nervous system in adults.Although chemotherapy is an important component of glioblastoma treatment,its effectiveness remains unsatisfactory.Due to multiple immunosuppressive mechanisms,glioblastoma immunotherapy has not been effective in treating many patients as a result of the clinical breakthroughs in the field.Therefore,the development of cancer immunotherapy relies on the understanding of how tumors interact with the immune system and the analysis of their molecular determinants.This study identified the key interactions between immune cells in the glioma microenvironment using RNA microarrays and single-cell sequencing.Methods:First,we screened differentially expressed genes in tumor and control samples from GSE29796 and GSE50161 datasets using GEO2R.All differentially expressed genes were used to perform enrichment analysis and construct protein-protein interaction topological analysis to analyze the interaction between proteins.Using single-cell RNA sequencing data from the GSE162631 database,we identified immune cell types within the glioblastoma microenvironment,and validated the hub gene expression in these cells.In addition,based on the GEPIA and TIMER databases,hub genes were investigated and compared with immune infiltration to determine differential expression.Finally,CellChat was used to visualize the gene expression distribution and cell-to-cell communication analysis of the proteins between different types of cells.Results:We found that monocytes/macrophages may communicate with each other in the tumor microenvironment through MIF-(CD74+CXCR4)and MIF-(CD74+CD44).In addition,our study indicated that celastrol has the ability to inhibit inflammatory factors expression by MIF/CD74 signaling pathway in U87 cells.Conclusion:This study improved the effectiveness of cancer immunotherapy strategies and developed new ideas for immunotherapy that can be applied to glioblastoma. 展开更多
关键词 GLIOBLASTOMA monocytes/macrophages single-cell RNA sequencing MIF/CD74 signaling pathway CELASTROL
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Is Chemokine Receptor CCR9 Required for Synovitis in Rheumatoid Arthritis? Deficiency of CCR9 in a Murine Model of Antigen-Induced Arthritis
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作者 Alison Cartwright Sophie King +1 位作者 Jim Middleton Oksana Kehoe 《Open Journal of Rheumatology and Autoimmune Diseases》 2012年第4期77-84,共8页
Objectives: Monocytes/macrophages accumulate in the synovial membrane in rheumatoid arthritis and play a key role in disease pathogenesis, contributing to inflammation, cartilage destruction and bone erosion. Identifi... Objectives: Monocytes/macrophages accumulate in the synovial membrane in rheumatoid arthritis and play a key role in disease pathogenesis, contributing to inflammation, cartilage destruction and bone erosion. Identification of molecules involved in monocyte/macrophage recruitment in inflammation is crucial for development of therapeutic interventions. Chemokine receptor CCR9 is up-regulated on these cells in peripheral blood and synovium of rheumatoid patients. This study investigated the course of antigen-induced arthritis in CCR9 deficient C57BL/6 mice in comparison to wild type animals to determine whether CCR9 is critical for disease severity and progression. Methods: Methylated bovine serum albumin was used for induction of uni-lateral arthritis by direct injection into the knee joints of preimmunized animals. Arthritis is confined to the injected joint allowing comparison with the normal opposing joint. Clinical severity of arthritis was assessed by measuring swelling in the arthritic joint in comparison to the normal joint. Histological analysis was performed to assess the extent of leukocyte infiltration and cartilage depletion. Results: Levels of swelling were not significantly different between wild type and CCR9 deficient mice. Similarly there was no significant difference in histological severity of arthritis when comparing CCR9-deficient mice to wild type mice. Conclusions: CCR9 was not required for development of synovial inflammation and cartilage destruction in the anti-gen-induced model of arthritis in C57BL/6 mice in this study. This may reflect a true lack of a pathogenic role of CCR9 on monocyte/macrophage function in vivo or it may reflect differences in the current antigen-induced arthritis model when compared to human RA. 展开更多
关键词 CHEMOKINE Receptor CCR9 RHEUMATOID ARTHRITIS Inflammation Antigen-Induced ARTHRITIS Mouse Mod-el monocytes/macrophages
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