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Front Immunol. 2018 Feb 9;9:176. doi: 10.3389/fimmu.2018.00176. eCollection 2018.

T-Cell Metabolism in Hematopoietic Cell Transplantation.

Author information

1
Department of Microbiology and Immunology, Medical University of South Carolina, Charleston, SC, United States.
2
Department of Pediatric Ematology-Oncology, Medical University of South Carolina, Charleston, SC, United States.
3
Department of Medicine, Medical University of South Carolina, Charleston, SC, United States.

Abstract

Metabolism, including catabolism and anabolism, is a basic cellular process necessary for cell survival. T lymphocytes have a distinct metabolism that can determine both fate and function. T-cell activation depends on glycolysis to obtain materials and energy for proliferation and effector function. Importantly, T cells utilize different metabolic processes under different conditions and diseases. Allogeneic hematopoietic cell transplantation (allo-HCT) is a classic immunotherapy for hematological malignancies; however, the development of graft-versus-host disease (GVHD) is a major factor limiting the success of allo-HCT. T cells in the donor graft drive GVHD by mounting a robust immunological attack against recipient normal tissues. Hence, understanding T-cell metabolism after allo-HCT would provide potential metabolic targets for the control of GVHD and primary tumor relapse. The purpose of the current review is to highlight the key metabolic pathways involved in alloantigen-activated T cells and to discuss how manipulating these pathways can serve as potential new therapeutic strategies to induce immune tolerance after allo-transplantation. We will also summarize the recent progress in regulating T-cell metabolism in bone marrow transplantation by targeting novel metabolic regulators or immune checkpoint molecules.

KEYWORDS:

T cell; glycolysis; graft-versus-host disease; hematopoietic stem cell transplantation; metabolism

PMID:
29479351
PMCID:
PMC5811499
DOI:
10.3389/fimmu.2018.00176
[Indexed for MEDLINE]
Free PMC Article

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