Protein Kinase Lck

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Judith Bezgovsek - One of the best experts on this subject based on the ideXlab platform.

  • CEACAM1 promotes CD8 + T cell responses and improves control of a chronic viral infection
    Nature communications, 2018
    Co-Authors: Vishal Khairnar, Vikas Duhan, Ashwini M Patil, Fan Zhou, Hilal Bhat, Christine Thoens, Piyush Sharma, Tom Adomati, Sarah-kim Friendrich, Judith Bezgovsek
    Abstract:

    Dysfunction of CD8+ T cells can lead to the development of chronic viral infection. Identifying mechanisms responsible for such T cell dysfunction is therefore of great importance to understand how to prevent persistent viral infection. Here we show using lymphocytic choriomeningitis virus (LCMV) infection that carcinoembryonic antigen-related cell adhesion molecule 1 (CEACAM1) is fundamental for recruiting lymphocyte-specific Protein Kinase (Lck) into the T cell receptor complex to form an efficient immunological synapse. CEACAM1 is essential for activation of CD8+ T cells, and the absence of CEACAM1 on virus-specific CD8+ T cells limits the antiviral CD8+ T cell response. Treatment with anti-CEACAM1 antibody stabilizes Lck in the immunological synapse, prevents CD8+ T cell exhaustion, and improves control of virus infection in vivo. Treatment of human virus-specific CD8+ T cells with anti-CEACAM1 antibody similarly enhances their proliferation. We conclude that CEACAM1 is an important regulator of virus-specific CD8+ T cell functions in mice and humans and represents a promising therapeutic target for modulating CD8+ T cells.

  • CEACAM1 promotes CD8^+ T cell responses and improves control of a chronic viral infection
    Nature Communications, 2018
    Co-Authors: Vishal Khairnar, Vikas Duhan, Ashwini M Patil, Fan Zhou, Hilal Bhat, Christine Thoens, Piyush Sharma, Tom Adomati, Sarah-kim Friendrich, Judith Bezgovsek
    Abstract:

    Chronic viral infections are frequently associated with the dysfunction of CD8^+ T cells which includes loss of function and results in CD8^+ T cell exhaustion. Here the authors show a role of CEACAM1 in promoting responsive CD8^+ T cells in the context of a chronic lymphocytic choriomeningitis virus (LCMV) infection model. Dysfunction of CD8^+ T cells can lead to the development of chronic viral infection. Identifying mechanisms responsible for such T cell dysfunction is therefore of great importance to understand how to prevent persistent viral infection. Here we show using lymphocytic choriomeningitis virus (LCMV) infection that carcinoembryonic antigen-related cell adhesion molecule 1 (CEACAM1) is fundamental for recruiting lymphocyte-specific Protein Kinase (Lck) into the T cell receptor complex to form an efficient immunological synapse. CEACAM1 is essential for activation of CD8^+ T cells, and the absence of CEACAM1 on virus-specific CD8^+ T cells limits the antiviral CD8^+ T cell response. Treatment with anti-CEACAM1 antibody stabilizes Lck in the immunological synapse, prevents CD8^+ T cell exhaustion, and improves control of virus infection in vivo. Treatment of human virus-specific CD8^+ T cells with anti-CEACAM1 antibody similarly enhances their proliferation. We conclude that CEACAM1 is an important regulator of virus-specific CD8^+ T cell functions in mice and humans and represents a promising therapeutic target for modulating CD8^+ T cells.

Vishal Khairnar - One of the best experts on this subject based on the ideXlab platform.

  • CEACAM1 promotes CD8 + T cell responses and improves control of a chronic viral infection
    Nature communications, 2018
    Co-Authors: Vishal Khairnar, Vikas Duhan, Ashwini M Patil, Fan Zhou, Hilal Bhat, Christine Thoens, Piyush Sharma, Tom Adomati, Sarah-kim Friendrich, Judith Bezgovsek
    Abstract:

    Dysfunction of CD8+ T cells can lead to the development of chronic viral infection. Identifying mechanisms responsible for such T cell dysfunction is therefore of great importance to understand how to prevent persistent viral infection. Here we show using lymphocytic choriomeningitis virus (LCMV) infection that carcinoembryonic antigen-related cell adhesion molecule 1 (CEACAM1) is fundamental for recruiting lymphocyte-specific Protein Kinase (Lck) into the T cell receptor complex to form an efficient immunological synapse. CEACAM1 is essential for activation of CD8+ T cells, and the absence of CEACAM1 on virus-specific CD8+ T cells limits the antiviral CD8+ T cell response. Treatment with anti-CEACAM1 antibody stabilizes Lck in the immunological synapse, prevents CD8+ T cell exhaustion, and improves control of virus infection in vivo. Treatment of human virus-specific CD8+ T cells with anti-CEACAM1 antibody similarly enhances their proliferation. We conclude that CEACAM1 is an important regulator of virus-specific CD8+ T cell functions in mice and humans and represents a promising therapeutic target for modulating CD8+ T cells.

  • CEACAM1 promotes CD8^+ T cell responses and improves control of a chronic viral infection
    Nature Communications, 2018
    Co-Authors: Vishal Khairnar, Vikas Duhan, Ashwini M Patil, Fan Zhou, Hilal Bhat, Christine Thoens, Piyush Sharma, Tom Adomati, Sarah-kim Friendrich, Judith Bezgovsek
    Abstract:

    Chronic viral infections are frequently associated with the dysfunction of CD8^+ T cells which includes loss of function and results in CD8^+ T cell exhaustion. Here the authors show a role of CEACAM1 in promoting responsive CD8^+ T cells in the context of a chronic lymphocytic choriomeningitis virus (LCMV) infection model. Dysfunction of CD8^+ T cells can lead to the development of chronic viral infection. Identifying mechanisms responsible for such T cell dysfunction is therefore of great importance to understand how to prevent persistent viral infection. Here we show using lymphocytic choriomeningitis virus (LCMV) infection that carcinoembryonic antigen-related cell adhesion molecule 1 (CEACAM1) is fundamental for recruiting lymphocyte-specific Protein Kinase (Lck) into the T cell receptor complex to form an efficient immunological synapse. CEACAM1 is essential for activation of CD8^+ T cells, and the absence of CEACAM1 on virus-specific CD8^+ T cells limits the antiviral CD8^+ T cell response. Treatment with anti-CEACAM1 antibody stabilizes Lck in the immunological synapse, prevents CD8^+ T cell exhaustion, and improves control of virus infection in vivo. Treatment of human virus-specific CD8^+ T cells with anti-CEACAM1 antibody similarly enhances their proliferation. We conclude that CEACAM1 is an important regulator of virus-specific CD8^+ T cell functions in mice and humans and represents a promising therapeutic target for modulating CD8^+ T cells.

Christine Thoens - One of the best experts on this subject based on the ideXlab platform.

  • CEACAM1 promotes CD8 + T cell responses and improves control of a chronic viral infection
    Nature communications, 2018
    Co-Authors: Vishal Khairnar, Vikas Duhan, Ashwini M Patil, Fan Zhou, Hilal Bhat, Christine Thoens, Piyush Sharma, Tom Adomati, Sarah-kim Friendrich, Judith Bezgovsek
    Abstract:

    Dysfunction of CD8+ T cells can lead to the development of chronic viral infection. Identifying mechanisms responsible for such T cell dysfunction is therefore of great importance to understand how to prevent persistent viral infection. Here we show using lymphocytic choriomeningitis virus (LCMV) infection that carcinoembryonic antigen-related cell adhesion molecule 1 (CEACAM1) is fundamental for recruiting lymphocyte-specific Protein Kinase (Lck) into the T cell receptor complex to form an efficient immunological synapse. CEACAM1 is essential for activation of CD8+ T cells, and the absence of CEACAM1 on virus-specific CD8+ T cells limits the antiviral CD8+ T cell response. Treatment with anti-CEACAM1 antibody stabilizes Lck in the immunological synapse, prevents CD8+ T cell exhaustion, and improves control of virus infection in vivo. Treatment of human virus-specific CD8+ T cells with anti-CEACAM1 antibody similarly enhances their proliferation. We conclude that CEACAM1 is an important regulator of virus-specific CD8+ T cell functions in mice and humans and represents a promising therapeutic target for modulating CD8+ T cells.

  • CEACAM1 promotes CD8^+ T cell responses and improves control of a chronic viral infection
    Nature Communications, 2018
    Co-Authors: Vishal Khairnar, Vikas Duhan, Ashwini M Patil, Fan Zhou, Hilal Bhat, Christine Thoens, Piyush Sharma, Tom Adomati, Sarah-kim Friendrich, Judith Bezgovsek
    Abstract:

    Chronic viral infections are frequently associated with the dysfunction of CD8^+ T cells which includes loss of function and results in CD8^+ T cell exhaustion. Here the authors show a role of CEACAM1 in promoting responsive CD8^+ T cells in the context of a chronic lymphocytic choriomeningitis virus (LCMV) infection model. Dysfunction of CD8^+ T cells can lead to the development of chronic viral infection. Identifying mechanisms responsible for such T cell dysfunction is therefore of great importance to understand how to prevent persistent viral infection. Here we show using lymphocytic choriomeningitis virus (LCMV) infection that carcinoembryonic antigen-related cell adhesion molecule 1 (CEACAM1) is fundamental for recruiting lymphocyte-specific Protein Kinase (Lck) into the T cell receptor complex to form an efficient immunological synapse. CEACAM1 is essential for activation of CD8^+ T cells, and the absence of CEACAM1 on virus-specific CD8^+ T cells limits the antiviral CD8^+ T cell response. Treatment with anti-CEACAM1 antibody stabilizes Lck in the immunological synapse, prevents CD8^+ T cell exhaustion, and improves control of virus infection in vivo. Treatment of human virus-specific CD8^+ T cells with anti-CEACAM1 antibody similarly enhances their proliferation. We conclude that CEACAM1 is an important regulator of virus-specific CD8^+ T cell functions in mice and humans and represents a promising therapeutic target for modulating CD8^+ T cells.

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

  • CEACAM1 promotes CD8 + T cell responses and improves control of a chronic viral infection
    Nature communications, 2018
    Co-Authors: Vishal Khairnar, Vikas Duhan, Ashwini M Patil, Fan Zhou, Hilal Bhat, Christine Thoens, Piyush Sharma, Tom Adomati, Sarah-kim Friendrich, Judith Bezgovsek
    Abstract:

    Dysfunction of CD8+ T cells can lead to the development of chronic viral infection. Identifying mechanisms responsible for such T cell dysfunction is therefore of great importance to understand how to prevent persistent viral infection. Here we show using lymphocytic choriomeningitis virus (LCMV) infection that carcinoembryonic antigen-related cell adhesion molecule 1 (CEACAM1) is fundamental for recruiting lymphocyte-specific Protein Kinase (Lck) into the T cell receptor complex to form an efficient immunological synapse. CEACAM1 is essential for activation of CD8+ T cells, and the absence of CEACAM1 on virus-specific CD8+ T cells limits the antiviral CD8+ T cell response. Treatment with anti-CEACAM1 antibody stabilizes Lck in the immunological synapse, prevents CD8+ T cell exhaustion, and improves control of virus infection in vivo. Treatment of human virus-specific CD8+ T cells with anti-CEACAM1 antibody similarly enhances their proliferation. We conclude that CEACAM1 is an important regulator of virus-specific CD8+ T cell functions in mice and humans and represents a promising therapeutic target for modulating CD8+ T cells.

  • CEACAM1 promotes CD8^+ T cell responses and improves control of a chronic viral infection
    Nature Communications, 2018
    Co-Authors: Vishal Khairnar, Vikas Duhan, Ashwini M Patil, Fan Zhou, Hilal Bhat, Christine Thoens, Piyush Sharma, Tom Adomati, Sarah-kim Friendrich, Judith Bezgovsek
    Abstract:

    Chronic viral infections are frequently associated with the dysfunction of CD8^+ T cells which includes loss of function and results in CD8^+ T cell exhaustion. Here the authors show a role of CEACAM1 in promoting responsive CD8^+ T cells in the context of a chronic lymphocytic choriomeningitis virus (LCMV) infection model. Dysfunction of CD8^+ T cells can lead to the development of chronic viral infection. Identifying mechanisms responsible for such T cell dysfunction is therefore of great importance to understand how to prevent persistent viral infection. Here we show using lymphocytic choriomeningitis virus (LCMV) infection that carcinoembryonic antigen-related cell adhesion molecule 1 (CEACAM1) is fundamental for recruiting lymphocyte-specific Protein Kinase (Lck) into the T cell receptor complex to form an efficient immunological synapse. CEACAM1 is essential for activation of CD8^+ T cells, and the absence of CEACAM1 on virus-specific CD8^+ T cells limits the antiviral CD8^+ T cell response. Treatment with anti-CEACAM1 antibody stabilizes Lck in the immunological synapse, prevents CD8^+ T cell exhaustion, and improves control of virus infection in vivo. Treatment of human virus-specific CD8^+ T cells with anti-CEACAM1 antibody similarly enhances their proliferation. We conclude that CEACAM1 is an important regulator of virus-specific CD8^+ T cell functions in mice and humans and represents a promising therapeutic target for modulating CD8^+ T cells.

Vikas Duhan - One of the best experts on this subject based on the ideXlab platform.

  • CEACAM1 promotes CD8 + T cell responses and improves control of a chronic viral infection
    Nature communications, 2018
    Co-Authors: Vishal Khairnar, Vikas Duhan, Ashwini M Patil, Fan Zhou, Hilal Bhat, Christine Thoens, Piyush Sharma, Tom Adomati, Sarah-kim Friendrich, Judith Bezgovsek
    Abstract:

    Dysfunction of CD8+ T cells can lead to the development of chronic viral infection. Identifying mechanisms responsible for such T cell dysfunction is therefore of great importance to understand how to prevent persistent viral infection. Here we show using lymphocytic choriomeningitis virus (LCMV) infection that carcinoembryonic antigen-related cell adhesion molecule 1 (CEACAM1) is fundamental for recruiting lymphocyte-specific Protein Kinase (Lck) into the T cell receptor complex to form an efficient immunological synapse. CEACAM1 is essential for activation of CD8+ T cells, and the absence of CEACAM1 on virus-specific CD8+ T cells limits the antiviral CD8+ T cell response. Treatment with anti-CEACAM1 antibody stabilizes Lck in the immunological synapse, prevents CD8+ T cell exhaustion, and improves control of virus infection in vivo. Treatment of human virus-specific CD8+ T cells with anti-CEACAM1 antibody similarly enhances their proliferation. We conclude that CEACAM1 is an important regulator of virus-specific CD8+ T cell functions in mice and humans and represents a promising therapeutic target for modulating CD8+ T cells.

  • CEACAM1 promotes CD8^+ T cell responses and improves control of a chronic viral infection
    Nature Communications, 2018
    Co-Authors: Vishal Khairnar, Vikas Duhan, Ashwini M Patil, Fan Zhou, Hilal Bhat, Christine Thoens, Piyush Sharma, Tom Adomati, Sarah-kim Friendrich, Judith Bezgovsek
    Abstract:

    Chronic viral infections are frequently associated with the dysfunction of CD8^+ T cells which includes loss of function and results in CD8^+ T cell exhaustion. Here the authors show a role of CEACAM1 in promoting responsive CD8^+ T cells in the context of a chronic lymphocytic choriomeningitis virus (LCMV) infection model. Dysfunction of CD8^+ T cells can lead to the development of chronic viral infection. Identifying mechanisms responsible for such T cell dysfunction is therefore of great importance to understand how to prevent persistent viral infection. Here we show using lymphocytic choriomeningitis virus (LCMV) infection that carcinoembryonic antigen-related cell adhesion molecule 1 (CEACAM1) is fundamental for recruiting lymphocyte-specific Protein Kinase (Lck) into the T cell receptor complex to form an efficient immunological synapse. CEACAM1 is essential for activation of CD8^+ T cells, and the absence of CEACAM1 on virus-specific CD8^+ T cells limits the antiviral CD8^+ T cell response. Treatment with anti-CEACAM1 antibody stabilizes Lck in the immunological synapse, prevents CD8^+ T cell exhaustion, and improves control of virus infection in vivo. Treatment of human virus-specific CD8^+ T cells with anti-CEACAM1 antibody similarly enhances their proliferation. We conclude that CEACAM1 is an important regulator of virus-specific CD8^+ T cell functions in mice and humans and represents a promising therapeutic target for modulating CD8^+ T cells.