The Experts below are selected from a list of 24585 Experts worldwide ranked by ideXlab platform

Zhihai Qin - One of the best experts on this subject based on the ideXlab platform.

  • abstract 1616 s100a4 blockage alleviates agonistic anti cd137 antibody induced Liver Pathology without disruption of anti tumor immunity
    Cancer Research, 2017
    Co-Authors: Jinhua Zhang, Kun Song, Zhihai Qin
    Abstract:

    Liver-related autoimmune toxicities triggered by anti-CD137 agonist antibodies have greatly limited their use in clinic applications. Here we found that anti-CD137 monoclonal antibody (mAb) treatment in mice induced the infiltration of a large number of S100A4+ macrophages into the Liver. Depletion of these cells or deficiency of S100A4 decreased inflammatory cytokine profiles, and drastically reduced the number of Liver pathogenic CD8+ T cells. Mechanistically, soluble S100A4 directly activated the Akt pathway and specifically prolonged CD8+ T cell survival. Interestingly, one S100A4 neutralizing monoclonal antibody selectively alleviated Liver abnormalities but did not affect the anti-tumor immunity induced by anti-CD137 therapy. Thus, our study presents a novel molecular link to the Liver Pathology induced by an immune stimulatory antibody, and proposes that combinational immunotherapies targeting those pathways could potentially elicit optimal anti-tumor immunity with minimal side effects. Note: This abstract was not presented at the meeting. Citation Format: Jinhua Zhang, Kun Song, Zhihai Qin. S100A4 blockage alleviates agonistic anti-CD137 antibody induced Liver Pathology without disruption of anti-tumor immunity [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2017; 2017 Apr 1-5; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2017;77(13 Suppl):Abstract nr 1616. doi:10.1158/1538-7445.AM2017-1616

  • s100a4 blockage alleviates agonistic anti cd137 antibody induced Liver Pathology without disruption of antitumor immunity
    OncoImmunology, 2017
    Co-Authors: Jinhua Zhang, Zhihai Qin, Kun Song, Jun Wang, Shuangqing Liu, Chengliang Dai, Lieping Chen, Shengdian Wang
    Abstract:

    Liver-related autoimmune toxicities triggered by agonistic anti-CD137 antibodies have greatly limited their use in clinical applications. Here, we found that anti-CD137 monoclonal antibody (mAb) treatment in mice induced the infiltration of a large number of S100A4+ macrophages into the Liver. Depletion of these cells or deficiency of S100A4 decreased inflammatory cytokine profiles and drastically reduced the number of Liver pathogenic CD8+ T cells. Mechanistically, soluble S100A4 directly activated the Akt pathway and specifically prolonged CD8+ T cell survival. Interestingly, one S100A4 neutralizing mAb selectively alleviated Liver abnormalities but did not affect the antitumor immunity induced by anti-CD137 mAb therapy. Thus, our study presents a novel molecular link to the Liver Pathology induced by an immune stimulatory antibody and proposes that combinational immunotherapies targeting those pathways could potentially elicit optimal antitumor immunity with minimal side effects.

Feng Liu - One of the best experts on this subject based on the ideXlab platform.

  • IL-7 suppresses macrophage autophagy and promotes Liver Pathology in Schistosoma japonicum-infected mice.
    Journal of cellular and molecular medicine, 2018
    Co-Authors: Jifeng Zhu, Xiaojun Chen, Sha Zhou, Weiwei Zhang, Lina Zhang, Ming Xiao, Hui Bai, Feng Liu
    Abstract:

    In schistosomiasis japonica and mansoni, parasite eggs trapped in host Liver elicit severe Liver granulomatous inflammation that subsequently leads to periportal fibrosis, portal hypertension, haemorrhage or even death. Macrophages are critical for granuloma formation and the development of Liver fibrosis during schistosomiasis. However, whether the aberrant regulation of macrophage autophagy has an effect on the development of Liver immunoPathology in schistosomiasis remains to be elucidated. In this study, we showed that Schistosoma japonicum (S. japonicum) egg antigen (SEA)-triggered macrophage autophagy limited the development of Pathology in host Liver. However, engagement of IL-7 receptor (IL-7R/CD127) on macrophages by S. japonicum infection-induced IL-7 significantly suppressed SEA-triggered macrophage autophagy, which led to an enhanced Liver Pathology. In addition, anti-IL-7 neutralizing antibody or anti-CD127 blocking antibody treatment increased macrophage autophagy and suppressed Liver Pathology. Finally, we demonstrated that IL-7 protects macrophage against SEA-induced autophagy through activation of AMP-activated protein kinase (AMPK). Our study reveals a novel role for IL-7 in macrophage autophagy and identifies AMPK as a novel downstream mediator of IL-7-IL-7R signalling and suggests that manipulation of macrophage autophagy by targeting IL-7-IL-7R signalling may have the potential to lead to improved treatment options for Liver pathogenesis in schistosomiasis.

  • Elevated serum antibody against Schistosoma japonicum HSP60 as a promising biomarker for Liver Pathology in schistosomiasis
    Scientific reports, 2017
    Co-Authors: Xiaojun Chen, Sha Zhou, Jifeng Zhu, Feng Liu, Dan-dan Lin
    Abstract:

    The Pathology associated with Schistosoma japonicum (S. japonicum) infection in humans is attributed to parasite egg-induced granulomatous inflammation and fibrosis in the host Liver. Currently, a marker that is reliable, cheap, less device-dependent, and can be easily and repeatedly used on a large scale to monitor the progression of Liver Pathology in schistosomiasis japonica endemic areas is lacking. The levels of serum S. japonicum heat shock protein 60 (SjHSP60)-specific IgG and its subtype antibodies in animals (mice and rabbits) or patients with schistosomiasis were measured by ELISA. Liver pathologies in mice and rabbits were evaluated by gross Pathology and histoPathology, and hepatic fibrosis in patients was examined with ultrasound imaging. The results revealed that the titers of the total IgG and subtype IgG1 anti-SjHSP60 antibodies were positively correlated with the severity of Liver Pathology after S. japonicum infection. Our findings indicate that the SjHSP60 IgG and IgG1 antibody levels can be used as potential candidate biomarkers for evaluation of Liver Pathology in schistosomiasis; however, validation remains to be explored in further work.

  • follicular helper t cells promote Liver Pathology in mice during schistosoma japonicum infection
    PLOS Pathogens, 2014
    Co-Authors: Xiaojun Chen, Sha Zhou, Jifeng Zhu, Weiwei Zhang, Xiaowei Yang, Xue Xue, Xiaoxiao Dong, Hsiangting Hsu, Wenjun Kong, Feng Liu
    Abstract:

    Following Schistosoma japonicum (S. japonicum) infection, granulomatous responses are induced by parasite eggs trapped in host organs, particular in the Liver, during the acute stage of disease. While excessive Liver granulomatous responses can lead to more severe fibrosis and circulatory impairment in chronically infected host. However, the exact mechanism of hepatic granuloma formation has remained obscure. In this study, we for the first time showed that follicular helper T (Tfh) cells are recruited to the Liver to upregulate hepatic granuloma formation and Liver injury in S. japonicum-infected mice, and identified a novel function of macrophages in Tfh cell induction. In addition, our results showed that the generation of Tfh cells driven by macrophages is dependent on cell-cell contact and the level of inducible costimulator ligand (ICOSL) on macrophages which is regulated by CD40-CD40L signaling. Our findings uncovered a previously unappreciated role for Tfh cells in Liver Pathology caused by S. japonicum infection in mice.

Xiaojun Chen - One of the best experts on this subject based on the ideXlab platform.

  • IL-7 suppresses macrophage autophagy and promotes Liver Pathology in Schistosoma japonicum-infected mice.
    Journal of cellular and molecular medicine, 2018
    Co-Authors: Jifeng Zhu, Xiaojun Chen, Sha Zhou, Weiwei Zhang, Lina Zhang, Ming Xiao, Hui Bai, Feng Liu
    Abstract:

    In schistosomiasis japonica and mansoni, parasite eggs trapped in host Liver elicit severe Liver granulomatous inflammation that subsequently leads to periportal fibrosis, portal hypertension, haemorrhage or even death. Macrophages are critical for granuloma formation and the development of Liver fibrosis during schistosomiasis. However, whether the aberrant regulation of macrophage autophagy has an effect on the development of Liver immunoPathology in schistosomiasis remains to be elucidated. In this study, we showed that Schistosoma japonicum (S. japonicum) egg antigen (SEA)-triggered macrophage autophagy limited the development of Pathology in host Liver. However, engagement of IL-7 receptor (IL-7R/CD127) on macrophages by S. japonicum infection-induced IL-7 significantly suppressed SEA-triggered macrophage autophagy, which led to an enhanced Liver Pathology. In addition, anti-IL-7 neutralizing antibody or anti-CD127 blocking antibody treatment increased macrophage autophagy and suppressed Liver Pathology. Finally, we demonstrated that IL-7 protects macrophage against SEA-induced autophagy through activation of AMP-activated protein kinase (AMPK). Our study reveals a novel role for IL-7 in macrophage autophagy and identifies AMPK as a novel downstream mediator of IL-7-IL-7R signalling and suggests that manipulation of macrophage autophagy by targeting IL-7-IL-7R signalling may have the potential to lead to improved treatment options for Liver pathogenesis in schistosomiasis.

  • Elevated serum antibody against Schistosoma japonicum HSP60 as a promising biomarker for Liver Pathology in schistosomiasis
    Scientific reports, 2017
    Co-Authors: Xiaojun Chen, Sha Zhou, Jifeng Zhu, Feng Liu, Dan-dan Lin
    Abstract:

    The Pathology associated with Schistosoma japonicum (S. japonicum) infection in humans is attributed to parasite egg-induced granulomatous inflammation and fibrosis in the host Liver. Currently, a marker that is reliable, cheap, less device-dependent, and can be easily and repeatedly used on a large scale to monitor the progression of Liver Pathology in schistosomiasis japonica endemic areas is lacking. The levels of serum S. japonicum heat shock protein 60 (SjHSP60)-specific IgG and its subtype antibodies in animals (mice and rabbits) or patients with schistosomiasis were measured by ELISA. Liver pathologies in mice and rabbits were evaluated by gross Pathology and histoPathology, and hepatic fibrosis in patients was examined with ultrasound imaging. The results revealed that the titers of the total IgG and subtype IgG1 anti-SjHSP60 antibodies were positively correlated with the severity of Liver Pathology after S. japonicum infection. Our findings indicate that the SjHSP60 IgG and IgG1 antibody levels can be used as potential candidate biomarkers for evaluation of Liver Pathology in schistosomiasis; however, validation remains to be explored in further work.

  • follicular helper t cells promote Liver Pathology in mice during schistosoma japonicum infection
    PLOS Pathogens, 2014
    Co-Authors: Xiaojun Chen, Sha Zhou, Jifeng Zhu, Weiwei Zhang, Xiaowei Yang, Xue Xue, Xiaoxiao Dong, Hsiangting Hsu, Wenjun Kong, Feng Liu
    Abstract:

    Following Schistosoma japonicum (S. japonicum) infection, granulomatous responses are induced by parasite eggs trapped in host organs, particular in the Liver, during the acute stage of disease. While excessive Liver granulomatous responses can lead to more severe fibrosis and circulatory impairment in chronically infected host. However, the exact mechanism of hepatic granuloma formation has remained obscure. In this study, we for the first time showed that follicular helper T (Tfh) cells are recruited to the Liver to upregulate hepatic granuloma formation and Liver injury in S. japonicum-infected mice, and identified a novel function of macrophages in Tfh cell induction. In addition, our results showed that the generation of Tfh cells driven by macrophages is dependent on cell-cell contact and the level of inducible costimulator ligand (ICOSL) on macrophages which is regulated by CD40-CD40L signaling. Our findings uncovered a previously unappreciated role for Tfh cells in Liver Pathology caused by S. japonicum infection in mice.

Jifeng Zhu - One of the best experts on this subject based on the ideXlab platform.

  • IL-7 suppresses macrophage autophagy and promotes Liver Pathology in Schistosoma japonicum-infected mice.
    Journal of cellular and molecular medicine, 2018
    Co-Authors: Jifeng Zhu, Xiaojun Chen, Sha Zhou, Weiwei Zhang, Lina Zhang, Ming Xiao, Hui Bai, Feng Liu
    Abstract:

    In schistosomiasis japonica and mansoni, parasite eggs trapped in host Liver elicit severe Liver granulomatous inflammation that subsequently leads to periportal fibrosis, portal hypertension, haemorrhage or even death. Macrophages are critical for granuloma formation and the development of Liver fibrosis during schistosomiasis. However, whether the aberrant regulation of macrophage autophagy has an effect on the development of Liver immunoPathology in schistosomiasis remains to be elucidated. In this study, we showed that Schistosoma japonicum (S. japonicum) egg antigen (SEA)-triggered macrophage autophagy limited the development of Pathology in host Liver. However, engagement of IL-7 receptor (IL-7R/CD127) on macrophages by S. japonicum infection-induced IL-7 significantly suppressed SEA-triggered macrophage autophagy, which led to an enhanced Liver Pathology. In addition, anti-IL-7 neutralizing antibody or anti-CD127 blocking antibody treatment increased macrophage autophagy and suppressed Liver Pathology. Finally, we demonstrated that IL-7 protects macrophage against SEA-induced autophagy through activation of AMP-activated protein kinase (AMPK). Our study reveals a novel role for IL-7 in macrophage autophagy and identifies AMPK as a novel downstream mediator of IL-7-IL-7R signalling and suggests that manipulation of macrophage autophagy by targeting IL-7-IL-7R signalling may have the potential to lead to improved treatment options for Liver pathogenesis in schistosomiasis.

  • Elevated serum antibody against Schistosoma japonicum HSP60 as a promising biomarker for Liver Pathology in schistosomiasis
    Scientific reports, 2017
    Co-Authors: Xiaojun Chen, Sha Zhou, Jifeng Zhu, Feng Liu, Dan-dan Lin
    Abstract:

    The Pathology associated with Schistosoma japonicum (S. japonicum) infection in humans is attributed to parasite egg-induced granulomatous inflammation and fibrosis in the host Liver. Currently, a marker that is reliable, cheap, less device-dependent, and can be easily and repeatedly used on a large scale to monitor the progression of Liver Pathology in schistosomiasis japonica endemic areas is lacking. The levels of serum S. japonicum heat shock protein 60 (SjHSP60)-specific IgG and its subtype antibodies in animals (mice and rabbits) or patients with schistosomiasis were measured by ELISA. Liver pathologies in mice and rabbits were evaluated by gross Pathology and histoPathology, and hepatic fibrosis in patients was examined with ultrasound imaging. The results revealed that the titers of the total IgG and subtype IgG1 anti-SjHSP60 antibodies were positively correlated with the severity of Liver Pathology after S. japonicum infection. Our findings indicate that the SjHSP60 IgG and IgG1 antibody levels can be used as potential candidate biomarkers for evaluation of Liver Pathology in schistosomiasis; however, validation remains to be explored in further work.

  • follicular helper t cells promote Liver Pathology in mice during schistosoma japonicum infection
    PLOS Pathogens, 2014
    Co-Authors: Xiaojun Chen, Sha Zhou, Jifeng Zhu, Weiwei Zhang, Xiaowei Yang, Xue Xue, Xiaoxiao Dong, Hsiangting Hsu, Wenjun Kong, Feng Liu
    Abstract:

    Following Schistosoma japonicum (S. japonicum) infection, granulomatous responses are induced by parasite eggs trapped in host organs, particular in the Liver, during the acute stage of disease. While excessive Liver granulomatous responses can lead to more severe fibrosis and circulatory impairment in chronically infected host. However, the exact mechanism of hepatic granuloma formation has remained obscure. In this study, we for the first time showed that follicular helper T (Tfh) cells are recruited to the Liver to upregulate hepatic granuloma formation and Liver injury in S. japonicum-infected mice, and identified a novel function of macrophages in Tfh cell induction. In addition, our results showed that the generation of Tfh cells driven by macrophages is dependent on cell-cell contact and the level of inducible costimulator ligand (ICOSL) on macrophages which is regulated by CD40-CD40L signaling. Our findings uncovered a previously unappreciated role for Tfh cells in Liver Pathology caused by S. japonicum infection in mice.

Sha Zhou - One of the best experts on this subject based on the ideXlab platform.

  • IL-7 suppresses macrophage autophagy and promotes Liver Pathology in Schistosoma japonicum-infected mice.
    Journal of cellular and molecular medicine, 2018
    Co-Authors: Jifeng Zhu, Xiaojun Chen, Sha Zhou, Weiwei Zhang, Lina Zhang, Ming Xiao, Hui Bai, Feng Liu
    Abstract:

    In schistosomiasis japonica and mansoni, parasite eggs trapped in host Liver elicit severe Liver granulomatous inflammation that subsequently leads to periportal fibrosis, portal hypertension, haemorrhage or even death. Macrophages are critical for granuloma formation and the development of Liver fibrosis during schistosomiasis. However, whether the aberrant regulation of macrophage autophagy has an effect on the development of Liver immunoPathology in schistosomiasis remains to be elucidated. In this study, we showed that Schistosoma japonicum (S. japonicum) egg antigen (SEA)-triggered macrophage autophagy limited the development of Pathology in host Liver. However, engagement of IL-7 receptor (IL-7R/CD127) on macrophages by S. japonicum infection-induced IL-7 significantly suppressed SEA-triggered macrophage autophagy, which led to an enhanced Liver Pathology. In addition, anti-IL-7 neutralizing antibody or anti-CD127 blocking antibody treatment increased macrophage autophagy and suppressed Liver Pathology. Finally, we demonstrated that IL-7 protects macrophage against SEA-induced autophagy through activation of AMP-activated protein kinase (AMPK). Our study reveals a novel role for IL-7 in macrophage autophagy and identifies AMPK as a novel downstream mediator of IL-7-IL-7R signalling and suggests that manipulation of macrophage autophagy by targeting IL-7-IL-7R signalling may have the potential to lead to improved treatment options for Liver pathogenesis in schistosomiasis.

  • Elevated serum antibody against Schistosoma japonicum HSP60 as a promising biomarker for Liver Pathology in schistosomiasis
    Scientific reports, 2017
    Co-Authors: Xiaojun Chen, Sha Zhou, Jifeng Zhu, Feng Liu, Dan-dan Lin
    Abstract:

    The Pathology associated with Schistosoma japonicum (S. japonicum) infection in humans is attributed to parasite egg-induced granulomatous inflammation and fibrosis in the host Liver. Currently, a marker that is reliable, cheap, less device-dependent, and can be easily and repeatedly used on a large scale to monitor the progression of Liver Pathology in schistosomiasis japonica endemic areas is lacking. The levels of serum S. japonicum heat shock protein 60 (SjHSP60)-specific IgG and its subtype antibodies in animals (mice and rabbits) or patients with schistosomiasis were measured by ELISA. Liver pathologies in mice and rabbits were evaluated by gross Pathology and histoPathology, and hepatic fibrosis in patients was examined with ultrasound imaging. The results revealed that the titers of the total IgG and subtype IgG1 anti-SjHSP60 antibodies were positively correlated with the severity of Liver Pathology after S. japonicum infection. Our findings indicate that the SjHSP60 IgG and IgG1 antibody levels can be used as potential candidate biomarkers for evaluation of Liver Pathology in schistosomiasis; however, validation remains to be explored in further work.

  • follicular helper t cells promote Liver Pathology in mice during schistosoma japonicum infection
    PLOS Pathogens, 2014
    Co-Authors: Xiaojun Chen, Sha Zhou, Jifeng Zhu, Weiwei Zhang, Xiaowei Yang, Xue Xue, Xiaoxiao Dong, Hsiangting Hsu, Wenjun Kong, Feng Liu
    Abstract:

    Following Schistosoma japonicum (S. japonicum) infection, granulomatous responses are induced by parasite eggs trapped in host organs, particular in the Liver, during the acute stage of disease. While excessive Liver granulomatous responses can lead to more severe fibrosis and circulatory impairment in chronically infected host. However, the exact mechanism of hepatic granuloma formation has remained obscure. In this study, we for the first time showed that follicular helper T (Tfh) cells are recruited to the Liver to upregulate hepatic granuloma formation and Liver injury in S. japonicum-infected mice, and identified a novel function of macrophages in Tfh cell induction. In addition, our results showed that the generation of Tfh cells driven by macrophages is dependent on cell-cell contact and the level of inducible costimulator ligand (ICOSL) on macrophages which is regulated by CD40-CD40L signaling. Our findings uncovered a previously unappreciated role for Tfh cells in Liver Pathology caused by S. japonicum infection in mice.