Research Topic

Strategies for Modulating T cell responses in Autoimmunity and Infection

About this Research Topic

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 cells 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.


Keywords: T cell modulation, Autoimmunity, Infection, Immune checkpoint, T cell, Treg


Important Note: All contributions to this Research Topic must be within the scope of the section and journal to which they are submitted, as defined in their mission statements. Frontiers reserves the right to guide an out-of-scope manuscript to a more suitable section or journal at any stage of peer review.

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 cells 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.


Keywords: T cell modulation, Autoimmunity, Infection, Immune checkpoint, T cell, Treg


Important Note: All contributions to this Research Topic must be within the scope of the section and journal to which they are submitted, as defined in their mission statements. Frontiers reserves the right to guide an out-of-scope manuscript to a more suitable section or journal at any stage of peer review.

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Submission Deadlines

15 February 2018 Abstract
15 June 2018 Manuscript

Participating Journals

Manuscripts can be submitted to this Research Topic via the following journals:

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Topic Editors

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Submission Deadlines

15 February 2018 Abstract
15 June 2018 Manuscript

Participating Journals

Manuscripts can be submitted to this Research Topic via the following journals:

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