The Experts below are selected from a list of 324456 Experts worldwide ranked by ideXlab platform

Mark A Petersen - One of the best experts on this subject based on the ideXlab platform.

  • blood coagulation protein fibrinogen promotes autoimmunity and demyelination via chemokine release and Antigen presentation
    Nature Communications, 2015
    Co-Authors: Mark A Petersen, Sara G Murray, Kim M Baeten, Anke Meyerfranke, Justin P Chan, Eirini Vagena, Catherine Bedard, Michael R Machado, Pamela Rios E Coronado, Thomas Prodhomme
    Abstract:

    Autoimmunity and macrophage recruitment into the central nervous system (CNS) are critical determinants of neuroinflammatory diseases. However, the mechanisms that drive immunological responses targeted to the CNS remain largely unknown. Here we show that fibrinogen, a central blood coagulation protein deposited in the CNS after blood-brain barrier disruption, induces encephalitogenic adaptive immune responses and peripheral macrophage recruitment into the CNS leading to demyelination. Fibrinogen stimulates a unique transcriptional signature in CD11b(+) Antigen-presenting cells inducing the recruitment and local CNS activation of myelin Antigen-specific Th1 cells. Fibrinogen depletion reduces Th1 cells in the multiple sclerosis model, experimental autoimmune encephalomyelitis. Major histocompatibility complex (MHC) II-dependent Antigen presentation, CXCL10- and CCL2-mediated recruitment of T cells and macrophages, respectively, are required for fibrinogen-induced encephalomyelitis. Inhibition of the fibrinogen receptor CD11b/CD18 protects from all immune and neuropathologic effects. Our results show that the final product of the coagulation cascade is a key determinant of CNS autoimmunity.

  • Blood coagulation protein fibrinogen promotes autoimmunity and demyelination via chemokine release and Antigen presentation
    Nature Communications, 2015
    Co-Authors: Jae Kyu Ryu, Mark A Petersen, Sara G Murray, Kim M Baeten, Justin P Chan, Eirini Vagena, Catherine Bedard, Michael R Machado, Anke Meyer-franke, Pamela E. Rios Coronado
    Abstract:

    Autoimmunity and macrophage recruitment into the central nervous system (CNS) are critical determinants of neuroinflammatory diseases. However, the mechanisms that drive immunological responses targeted to the CNS remain largely unknown. Here we show that fibrinogen, a central blood coagulation protein deposited in the CNS after blood–brain barrier disruption, induces encephalitogenic adaptive immune responses and peripheral macrophage recruitment into the CNS leading to demyelination. Fibrinogen stimulates a unique transcriptional signature in CD11b^+ Antigen-presenting cells inducing the recruitment and local CNS activation of myelin Antigen-specific Th1 cells. Fibrinogen depletion reduces Th1 cells in the multiple sclerosis model, experimental autoimmune encephalomyelitis. Major histocompatibility complex (MHC) II-dependent Antigen presentation, CXCL10- and CCL2-mediated recruitment of T cells and macrophages, respectively, are required for fibrinogen-induced encephalomyelitis. Inhibition of the fibrinogen receptor CD11b/CD18 protects from all immune and neuropathologic effects. Our results show that the final product of the coagulation cascade is a key determinant of CNS autoimmunity. Autoimmune brain inflammation is associated with activation of macrophages and microglia. Here the authors show that fibrinogen induces encephalitogenic T-cell activation and macrophage recruitment to the central nervous system, and promotes demyelination in a mouse model of multiple sclerosis.

Pamela E. Rios Coronado - One of the best experts on this subject based on the ideXlab platform.

  • Blood coagulation protein fibrinogen promotes autoimmunity and demyelination via chemokine release and Antigen presentation
    Nature Communications, 2015
    Co-Authors: Jae Kyu Ryu, Mark A Petersen, Sara G Murray, Kim M Baeten, Justin P Chan, Eirini Vagena, Catherine Bedard, Michael R Machado, Anke Meyer-franke, Pamela E. Rios Coronado
    Abstract:

    Autoimmunity and macrophage recruitment into the central nervous system (CNS) are critical determinants of neuroinflammatory diseases. However, the mechanisms that drive immunological responses targeted to the CNS remain largely unknown. Here we show that fibrinogen, a central blood coagulation protein deposited in the CNS after blood–brain barrier disruption, induces encephalitogenic adaptive immune responses and peripheral macrophage recruitment into the CNS leading to demyelination. Fibrinogen stimulates a unique transcriptional signature in CD11b^+ Antigen-presenting cells inducing the recruitment and local CNS activation of myelin Antigen-specific Th1 cells. Fibrinogen depletion reduces Th1 cells in the multiple sclerosis model, experimental autoimmune encephalomyelitis. Major histocompatibility complex (MHC) II-dependent Antigen presentation, CXCL10- and CCL2-mediated recruitment of T cells and macrophages, respectively, are required for fibrinogen-induced encephalomyelitis. Inhibition of the fibrinogen receptor CD11b/CD18 protects from all immune and neuropathologic effects. Our results show that the final product of the coagulation cascade is a key determinant of CNS autoimmunity. Autoimmune brain inflammation is associated with activation of macrophages and microglia. Here the authors show that fibrinogen induces encephalitogenic T-cell activation and macrophage recruitment to the central nervous system, and promotes demyelination in a mouse model of multiple sclerosis.

Thomas Prodhomme - One of the best experts on this subject based on the ideXlab platform.

  • blood coagulation protein fibrinogen promotes autoimmunity and demyelination via chemokine release and Antigen presentation
    Nature Communications, 2015
    Co-Authors: Mark A Petersen, Sara G Murray, Kim M Baeten, Anke Meyerfranke, Justin P Chan, Eirini Vagena, Catherine Bedard, Michael R Machado, Pamela Rios E Coronado, Thomas Prodhomme
    Abstract:

    Autoimmunity and macrophage recruitment into the central nervous system (CNS) are critical determinants of neuroinflammatory diseases. However, the mechanisms that drive immunological responses targeted to the CNS remain largely unknown. Here we show that fibrinogen, a central blood coagulation protein deposited in the CNS after blood-brain barrier disruption, induces encephalitogenic adaptive immune responses and peripheral macrophage recruitment into the CNS leading to demyelination. Fibrinogen stimulates a unique transcriptional signature in CD11b(+) Antigen-presenting cells inducing the recruitment and local CNS activation of myelin Antigen-specific Th1 cells. Fibrinogen depletion reduces Th1 cells in the multiple sclerosis model, experimental autoimmune encephalomyelitis. Major histocompatibility complex (MHC) II-dependent Antigen presentation, CXCL10- and CCL2-mediated recruitment of T cells and macrophages, respectively, are required for fibrinogen-induced encephalomyelitis. Inhibition of the fibrinogen receptor CD11b/CD18 protects from all immune and neuropathologic effects. Our results show that the final product of the coagulation cascade is a key determinant of CNS autoimmunity.

Justin P Chan - One of the best experts on this subject based on the ideXlab platform.

  • blood coagulation protein fibrinogen promotes autoimmunity and demyelination via chemokine release and Antigen presentation
    Nature Communications, 2015
    Co-Authors: Mark A Petersen, Sara G Murray, Kim M Baeten, Anke Meyerfranke, Justin P Chan, Eirini Vagena, Catherine Bedard, Michael R Machado, Pamela Rios E Coronado, Thomas Prodhomme
    Abstract:

    Autoimmunity and macrophage recruitment into the central nervous system (CNS) are critical determinants of neuroinflammatory diseases. However, the mechanisms that drive immunological responses targeted to the CNS remain largely unknown. Here we show that fibrinogen, a central blood coagulation protein deposited in the CNS after blood-brain barrier disruption, induces encephalitogenic adaptive immune responses and peripheral macrophage recruitment into the CNS leading to demyelination. Fibrinogen stimulates a unique transcriptional signature in CD11b(+) Antigen-presenting cells inducing the recruitment and local CNS activation of myelin Antigen-specific Th1 cells. Fibrinogen depletion reduces Th1 cells in the multiple sclerosis model, experimental autoimmune encephalomyelitis. Major histocompatibility complex (MHC) II-dependent Antigen presentation, CXCL10- and CCL2-mediated recruitment of T cells and macrophages, respectively, are required for fibrinogen-induced encephalomyelitis. Inhibition of the fibrinogen receptor CD11b/CD18 protects from all immune and neuropathologic effects. Our results show that the final product of the coagulation cascade is a key determinant of CNS autoimmunity.

  • Blood coagulation protein fibrinogen promotes autoimmunity and demyelination via chemokine release and Antigen presentation
    Nature Communications, 2015
    Co-Authors: Jae Kyu Ryu, Mark A Petersen, Sara G Murray, Kim M Baeten, Justin P Chan, Eirini Vagena, Catherine Bedard, Michael R Machado, Anke Meyer-franke, Pamela E. Rios Coronado
    Abstract:

    Autoimmunity and macrophage recruitment into the central nervous system (CNS) are critical determinants of neuroinflammatory diseases. However, the mechanisms that drive immunological responses targeted to the CNS remain largely unknown. Here we show that fibrinogen, a central blood coagulation protein deposited in the CNS after blood–brain barrier disruption, induces encephalitogenic adaptive immune responses and peripheral macrophage recruitment into the CNS leading to demyelination. Fibrinogen stimulates a unique transcriptional signature in CD11b^+ Antigen-presenting cells inducing the recruitment and local CNS activation of myelin Antigen-specific Th1 cells. Fibrinogen depletion reduces Th1 cells in the multiple sclerosis model, experimental autoimmune encephalomyelitis. Major histocompatibility complex (MHC) II-dependent Antigen presentation, CXCL10- and CCL2-mediated recruitment of T cells and macrophages, respectively, are required for fibrinogen-induced encephalomyelitis. Inhibition of the fibrinogen receptor CD11b/CD18 protects from all immune and neuropathologic effects. Our results show that the final product of the coagulation cascade is a key determinant of CNS autoimmunity. Autoimmune brain inflammation is associated with activation of macrophages and microglia. Here the authors show that fibrinogen induces encephalitogenic T-cell activation and macrophage recruitment to the central nervous system, and promotes demyelination in a mouse model of multiple sclerosis.

Eirini Vagena - One of the best experts on this subject based on the ideXlab platform.

  • blood coagulation protein fibrinogen promotes autoimmunity and demyelination via chemokine release and Antigen presentation
    Nature Communications, 2015
    Co-Authors: Mark A Petersen, Sara G Murray, Kim M Baeten, Anke Meyerfranke, Justin P Chan, Eirini Vagena, Catherine Bedard, Michael R Machado, Pamela Rios E Coronado, Thomas Prodhomme
    Abstract:

    Autoimmunity and macrophage recruitment into the central nervous system (CNS) are critical determinants of neuroinflammatory diseases. However, the mechanisms that drive immunological responses targeted to the CNS remain largely unknown. Here we show that fibrinogen, a central blood coagulation protein deposited in the CNS after blood-brain barrier disruption, induces encephalitogenic adaptive immune responses and peripheral macrophage recruitment into the CNS leading to demyelination. Fibrinogen stimulates a unique transcriptional signature in CD11b(+) Antigen-presenting cells inducing the recruitment and local CNS activation of myelin Antigen-specific Th1 cells. Fibrinogen depletion reduces Th1 cells in the multiple sclerosis model, experimental autoimmune encephalomyelitis. Major histocompatibility complex (MHC) II-dependent Antigen presentation, CXCL10- and CCL2-mediated recruitment of T cells and macrophages, respectively, are required for fibrinogen-induced encephalomyelitis. Inhibition of the fibrinogen receptor CD11b/CD18 protects from all immune and neuropathologic effects. Our results show that the final product of the coagulation cascade is a key determinant of CNS autoimmunity.

  • Blood coagulation protein fibrinogen promotes autoimmunity and demyelination via chemokine release and Antigen presentation
    Nature Communications, 2015
    Co-Authors: Jae Kyu Ryu, Mark A Petersen, Sara G Murray, Kim M Baeten, Justin P Chan, Eirini Vagena, Catherine Bedard, Michael R Machado, Anke Meyer-franke, Pamela E. Rios Coronado
    Abstract:

    Autoimmunity and macrophage recruitment into the central nervous system (CNS) are critical determinants of neuroinflammatory diseases. However, the mechanisms that drive immunological responses targeted to the CNS remain largely unknown. Here we show that fibrinogen, a central blood coagulation protein deposited in the CNS after blood–brain barrier disruption, induces encephalitogenic adaptive immune responses and peripheral macrophage recruitment into the CNS leading to demyelination. Fibrinogen stimulates a unique transcriptional signature in CD11b^+ Antigen-presenting cells inducing the recruitment and local CNS activation of myelin Antigen-specific Th1 cells. Fibrinogen depletion reduces Th1 cells in the multiple sclerosis model, experimental autoimmune encephalomyelitis. Major histocompatibility complex (MHC) II-dependent Antigen presentation, CXCL10- and CCL2-mediated recruitment of T cells and macrophages, respectively, are required for fibrinogen-induced encephalomyelitis. Inhibition of the fibrinogen receptor CD11b/CD18 protects from all immune and neuropathologic effects. Our results show that the final product of the coagulation cascade is a key determinant of CNS autoimmunity. Autoimmune brain inflammation is associated with activation of macrophages and microglia. Here the authors show that fibrinogen induces encephalitogenic T-cell activation and macrophage recruitment to the central nervous system, and promotes demyelination in a mouse model of multiple sclerosis.