The Experts below are selected from a list of 23535 Experts worldwide ranked by ideXlab platform
Xu Huan - One of the best experts on this subject based on the ideXlab platform.
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Involvement of CXCL16 Chemokine in immunological liver injury in mice
Chinese journal of immunology, 2004Co-Authors: Xu HuanAbstract:Objective:CXCL16 Chemokine,with both secretory and transmembrane forms,is a recently indentified to selectively chemoattract CXCR6 + T lymphocytes.To investigate the expression pattern of CXCL16 Chemokine and pathophysiological roles of anti CXCL16 antibody in injured liver induced by BCG and LPS.Methods:Expression of CXCL16 was detected in immunological liver injury induced by BCG and LPS,and neutralizing anti CXCL16 monoclonal antibody(mAb)was further administrated in vivo to investigate its roles in hepatic necrosis,expression of apoptosis molecules,infiltration of hepatic lymphocytes and survive rate of mice.The dominant hepatic T lymphocytes populations were also analyzed to study the mechanism of CXCL16 in liver injury.Conclusion:These findings suggest that CXCL16 might play an important role in massive hepatic necrosis in BCG LPS induced liver injury by recruitment of intrahepatic specific lymphocytes and regulation of injury related molecules expression.
Duck Cho - One of the best experts on this subject based on the ideXlab platform.
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Irradiation of breast cancer cells enhances CXCL16 ligand expression and induces the migration of natural killer cells expressing the CXCR6 receptor
Cytotherapy, 2016Co-Authors: Mee Sun Yoon, Chanh Tin Pham, Minh-trang Thi Phan, Dong-jun Shin, Youn-young Jang, Min Ho Park, Sang-ki Kim, Seokho Kim, Duck ChoAbstract:Abstract Background aims Few studies have examined the migration pattern of natural killer (NK) cells, especially after radiation treatment for cancer. We investigated whether irradiation can modulate the expression of Chemokines in cancer cells and the migration of NK cells to irradiated tumor cells. Methods The expression of Chemokine receptors (CXCR3, CXCR4 and CXCR6) on interleukin-2 (IL-2)/IL-15–activated NK cells was assessed using flow cytometry. Related Chemokine ligands (CXCL11, CXCL12 and CXCL16) in human breast cancer cell lines (MCF7, SKBR3 and MDA-MB231) irradiated at various doses were assessed using reverse transcription–polymerase chain reaction (RT-PCR), fluorescence-activated cell sorting (FACS) and enzyme-linked immunosorbent assay (ELISA). The cell-free culture supernatant was collected 96 h after irradiation of breast cancer cell lines for migration and blocking assays. Results The activated NK cells expressed CXCR6. Expression of the CXCR6 ligand CXCL16 increased in a time- and dose-dependent manner in all analyzed cancer cell lines. CXCL16 expression was statistically significantly enhanced in all breast cancer cell lines on day 3 after 20 Gy irradiation. Activated NK cells migration correlated with CXCL16 concentration ( R 2 = 0.91; P 0.0001). Significantly enhanced migration of NK cells to irradiated cancer cells was observed for a dose of 20 Gy in MCF7 ( P = 0.043) and SKBR3 ( P = 0.043) cells, but not in MDA-MB231 ( P = 0.225) cells. A blocking assay using a CXCR6 antibody showed a significant decrease in the migration of activated NK cells in all cancer cell lines. Conclusions Our data indicate that irradiation induces CXCL16 Chemokine expression in cancer cells and enhances the migration of activated NK cells expressing CXCR6 to irradiated breast cancer cells. These results suggest that radiation would improve the anti-tumor effect of NK cells through enhanced migration of NK cells to tumor site for the treatment of patients with breast cancer.
Qianqian Lei - One of the best experts on this subject based on the ideXlab platform.
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CXCR6/CXCL16 functions as a regulator in metastasis and progression of cancer.
Biochimica et biophysica acta, 2010Co-Authors: Ling Deng, Nian-yong Chen, Hong Zheng, Qianqian LeiAbstract:Metastasis is considered the obvious mark for most aggressive cancers. However, little is known about the molecular mechanism of the regulation of cancer metastasis. Recent evidence increasingly suggests that the interaction between Chemokines and Chemokine receptors is pivotal in the process of metastasis. The Chemokine receptor CXCR4 and its ligand CXCL12, for example, have been reported to play a vital role in cancer metastasis. Another Chemokine and Chemokine receptor pair, the CXCL16/CXCR6 axis, has been studied by several independent research groups. Here, we summarize recent advances in our knowledge of the function of CXC Chemokine receptor CXCR6 and its ligand CXCL16 in regulating metastasis and invasion of cancer. CXCR6 and CXCL16 are up-regulated in multiple cancer tissue types and cancer cell lines relative to normal tissues and cell lines. In addition, both CXCR6 and CXCL16 levels increase as tumor malignancy increases. Trans-membranous CXCL16 Chemokine reduces proliferation while soluble CXCL16 Chemokine enhances proliferation and migration. TM-CXCL16 functions as an inducer for lymphocyte build-up around tumor sites. High trans-membranous CXCL16 expression correlates with a good prognosis. Moreover, the Akt/mTOR signal pathway is involved in activating the CXCR6/CXCL16 axis. These findings suggest multiple opportunities for blocking the CXCR6/CXCL16 axis and the Akt/mTOR signal pathway in novel cancer therapies.
Vito Pistoia - One of the best experts on this subject based on the ideXlab platform.
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Soluble HLA-G modulates miRNA-210 and miRNA-451 expression in activated CD4+ T lymphocytes
International immunology, 2012Co-Authors: Fabio Morandi, Vito PistoiaAbstract:In this study, we have investigated the expression of 87 micro (mi)RNAs in activated CD4+ T cells cultured in the presence or absence of the immunoregulatory molecule soluble HLA-G (sHLA-G). We observed (i) a decreased miR-451 expression and (ii) an increased miR-210 expression in sHLA-G-treated CD4+ T cells. By transfecting CD4+ T cells with miR-210 and miR-451 mimics or inhibitors, we found that sHLA-G-mediated modulation of these miRNAs was not related to sHLA-G-mediated inhibition of (i) proliferation and (ii) CXCR3 expression in CD4+ T cells. Finally, we investigated the expression of 14 genes targeted by miR-210 or miR-451 in activated CD4+ T cells, treated or not with sHLA-G. We observed an increased expression of OSR-1 (odd-skipped related 1) and HBP-1 (HMG-box transcription factor 1) and a decreased expression of CXCL16 (Chemokine C-X-C motif ligand 16) and C11orf30 (chromosome 11 open reading frame 30) in sHLA-G-treated CD4+ T cells. In conclusion, sHLA-G triggered a modulation of miRNA expression that may in turn modulate downstream gene expression, thus affecting CD4+ T-cell function.
Xiong Si-don - One of the best experts on this subject based on the ideXlab platform.
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Protective role of CXCL16 antibody in murine immunological liver injury induced by BCG and LPS
Chinese journal of microbiology and immunology, 2005Co-Authors: Xiong Si-donAbstract:Objective To investigate the effects of CXCL16 antibody in murine immunological liver injury. Methods Mouse CXCL16 Chemokine was expressed and purified with prokaryotic expression systems. The chemotactic activity was analyzed by chemotaxis assay. CXCL16 antibody was prepared and purified. The specificity and neutralization of specific antibody were further detected with double immune diffuse. In immunological liver injury model induced by BCG and LPS, the neutralizing CXCL16 antibody was administrated in vivo, the hepatic necrosis, serum ALT level and survive rate were evaluated. Results Administration of CXCL16 antibody protected the mice from liver injury with a significant reduction of both ALT level and hepatic lesion. The life of animal was prolonged by CXCL16 treatment. Conclusion CXCL16 antibody has a potential protective role in murine liver injury induced by BCG and LPS.
