Research Topic

Tissue Resident Memory T Cells

About this Research Topic

Resident memory T cells (TRM), usually defined by the expression of the surface marker CD103, represent a new subset of long-lived memory T lymphocytes that reside in tissues, do not recirculate and therefore cannot be monitored by whole blood cell analyses. The identification of specific transcription factors required for their differentiation, such as Hobit and Blimp1, reinforced the fact that TRM constitute a specific T-cell lineage. However, they seem to derive from the same KLRG1-precursor T cells as those that give rise to long-lived memory T cells found in the circulation.

CD8+ TRM are highly protective during localized re-infections and display the capacity to directly kill pathogen-infected cells and to release cytokines and chemokines amplifying local recruitment of other innate and adaptive immune cells.

In cancer, the interaction of CD103 integrin with its ligand, the epithelial cell marker E-cadherin, favors the adhesion of TRM with epithelial tumor cells and participates in the potentiation of cytotoxicity and cytokine production of these cells. Interestingly, TRM are enriched in tumor-specific T cells and express high levels of inhibitory receptors, such as PD-1 and Tim-3, making them an attractive target for cancer immunotherapy based on immune checkpoint inhibitors (ICI). Induction of TRM has also been demonstrated to improve the efficacy of therapeutic cancer vaccines. The presence of intratumoral TRM in a series of human cancers, including lung, ovarian and bladder, was correlated with a better overall survival than the presence of other infiltrating immune cells.

This emerging field is thus extremely dynamic with rapid and recent accumulative results warranting a Research Topic on this subject. We welcome the submission of Review and Mini-Review articles that cover the following topics in this field:

1. Differentiation of TRM and the role of transcription factors in this process.
2. TRM cells and metabolism.
3. Differential roles of dendritic cells in the priming of TRM cells.
4. Role of inflammation and the microenvironment in the differentiation of TRM cells
5. Sub-populations of TRM cells depending on their location and function.
6. Localization of TRM cells and tissue niches.
7. CD4+ resident memory T cells.
8. TRM cells and allergy.
9. TRM cells and chronic infection.
10. Role of TRM in vaccines directed against infectious diseases.
11. Phenotype, function and TRM signature in cancer.
12. TRM as a prognostic marker in cancer.
13. TRM cells and response to cancer vaccine and immunotherapy based on immune checkpoint inhibitors.


Keywords: Immunology, memory T lymphocytes, differentiation, residency, cancer and infectious diseases


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.

Resident memory T cells (TRM), usually defined by the expression of the surface marker CD103, represent a new subset of long-lived memory T lymphocytes that reside in tissues, do not recirculate and therefore cannot be monitored by whole blood cell analyses. The identification of specific transcription factors required for their differentiation, such as Hobit and Blimp1, reinforced the fact that TRM constitute a specific T-cell lineage. However, they seem to derive from the same KLRG1-precursor T cells as those that give rise to long-lived memory T cells found in the circulation.

CD8+ TRM are highly protective during localized re-infections and display the capacity to directly kill pathogen-infected cells and to release cytokines and chemokines amplifying local recruitment of other innate and adaptive immune cells.

In cancer, the interaction of CD103 integrin with its ligand, the epithelial cell marker E-cadherin, favors the adhesion of TRM with epithelial tumor cells and participates in the potentiation of cytotoxicity and cytokine production of these cells. Interestingly, TRM are enriched in tumor-specific T cells and express high levels of inhibitory receptors, such as PD-1 and Tim-3, making them an attractive target for cancer immunotherapy based on immune checkpoint inhibitors (ICI). Induction of TRM has also been demonstrated to improve the efficacy of therapeutic cancer vaccines. The presence of intratumoral TRM in a series of human cancers, including lung, ovarian and bladder, was correlated with a better overall survival than the presence of other infiltrating immune cells.

This emerging field is thus extremely dynamic with rapid and recent accumulative results warranting a Research Topic on this subject. We welcome the submission of Review and Mini-Review articles that cover the following topics in this field:

1. Differentiation of TRM and the role of transcription factors in this process.
2. TRM cells and metabolism.
3. Differential roles of dendritic cells in the priming of TRM cells.
4. Role of inflammation and the microenvironment in the differentiation of TRM cells
5. Sub-populations of TRM cells depending on their location and function.
6. Localization of TRM cells and tissue niches.
7. CD4+ resident memory T cells.
8. TRM cells and allergy.
9. TRM cells and chronic infection.
10. Role of TRM in vaccines directed against infectious diseases.
11. Phenotype, function and TRM signature in cancer.
12. TRM as a prognostic marker in cancer.
13. TRM cells and response to cancer vaccine and immunotherapy based on immune checkpoint inhibitors.


Keywords: Immunology, memory T lymphocytes, differentiation, residency, cancer and infectious diseases


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

31 December 2017 Abstract
31 March 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

31 December 2017 Abstract
31 March 2018 Manuscript

Participating Journals

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

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