This research topic is the second volume in this series, Immune Tolerance Post Allogeneic Hematopoietic Cell Transplantation. Please see Volume I here.T cell responses are essential for protection against pathogens but can also be detrimental to the host. Therefore many overlapping mechanisms exist to prevent both the development of autoimmunity and excessive tissue damage during chronic infections.T cell differentiation and effector function are shaped by the integration of different signals from the environment. These signals are orchestrated through a variety of signaling receptors including the T cell receptor, activating (co-stimulatory molecules or cytokines), and inhibitory (checkpoint) receptors. Thus, the modulation of external signals could impact on the development or function of effector and/or regulatory T (Treg) cells. In pre-clinical human or animal studies, the manipulation of T cell function has been attempted via numerous different approaches. These include (i) immune checkpoint blockade (PD-1, PD-L1, Tim3 and/or CTLA-4 among others), (ii) alterations in metabolic pathways, and (iii) the utilization of biological agents such as hormones, cytokines, or neutralizing antibodies. Overall, these therapies aim to convert a pathological immune response into a protective one via the control or reprogramming of specific T cell subsets.This Research Topic aims to provide a comprehensive overview of the diverse strategies focused on modulating T cell function that aim to prevent or revert pathological immune responses against pathogens and self-antigens. We welcome the submission of Reviews, Mini-Reviews and Original Research articles that discuss a diversity of approaches aimed at modulating T cell responses in autoimmunity and infection, and how they have been or could be used to design novel immunotherapies.
This research topic is the second volume in this series, Immune Tolerance Post Allogeneic Hematopoietic Cell Transplantation. Please see Volume I here.T cell responses are essential for protection against pathogens but can also be detrimental to the host. Therefore many overlapping mechanisms exist to prevent both the development of autoimmunity and excessive tissue damage during chronic infections.T cell differentiation and effector function are shaped by the integration of different signals from the environment. These signals are orchestrated through a variety of signaling receptors including the T cell receptor, activating (co-stimulatory molecules or cytokines), and inhibitory (checkpoint) receptors. Thus, the modulation of external signals could impact on the development or function of effector and/or regulatory T (Treg) cells. In pre-clinical human or animal studies, the manipulation of T cell function has been attempted via numerous different approaches. These include (i) immune checkpoint blockade (PD-1, PD-L1, Tim3 and/or CTLA-4 among others), (ii) alterations in metabolic pathways, and (iii) the utilization of biological agents such as hormones, cytokines, or neutralizing antibodies. Overall, these therapies aim to convert a pathological immune response into a protective one via the control or reprogramming of specific T cell subsets.This Research Topic aims to provide a comprehensive overview of the diverse strategies focused on modulating T cell function that aim to prevent or revert pathological immune responses against pathogens and self-antigens. We welcome the submission of Reviews, Mini-Reviews and Original Research articles that discuss a diversity of approaches aimed at modulating T cell responses in autoimmunity and infection, and how they have been or could be used to design novel immunotherapies.