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Review
. 2017 Aug;31(4):335-347.
doi: 10.1007/s40259-017-0228-3.

Cell-Based Therapies with T Regulatory Cells

Mateusz Gliwiński  1 , Dorota Iwaszkiewicz-Grześ  1 , Piotr Trzonkowski  2
Affiliations
Review

Cell-Based Therapies with T Regulatory Cells

Mateusz Gliwiński et al. BioDrugs. 2017 Aug.

Abstract

CD4+CD25highFoxP3+ T regulatory cells (Tregs) are immunodominant suppressors in the immune system. Tregs use various mechanisms to control immune responses. Preclinical data from animal models have confirmed the huge therapeutic potential of Tregs in many immune-mediated diseases. Hence, these cells are now on the road to translation to cell therapy in the clinic as the first clinical trials are accomplished. To date, clinical research has involved mainly hematopoietic stem cell transplantations, solid organ transplantations, and autoimmunity. Despite difficulties with legislation and technical issues, treatment is constantly evolving and may soon represent a valid alternative for patients with diseases that are currently incurable. This review focuses on the basic and clinical experience with Tregs with adoptive transfer of these cells, primarily from clinical trials, as well as on perspectives on clinical use and technical problems with implementing the therapy.

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Conflict of interest statement

MG and DIG have no conflicts of interests. PT is a co-inventor of a patent related to the presented content and a stakeholder of the POLTREG venture. The Medical University of Gdańsk received payment for the license to the presented content.

Figures

Fig. 1
Fig. 1
Chosen mechanisms used by T regulatory cells (Tregs). I suppression of antigen presentation, induction of expression of IDO in DCs via the CTLA-4; II inhibition of activation of Th and cytotoxic T effector via cell-to-cell interactions, extracellularly produced adenosine via CD39, CD73 receptors; transferred cAMP and consumption of IL-2; III induction of apoptosis of mono/mac; IV inhibition of B-cell proliferation and induction of apoptosis via PD-1; V induction of apoptosis of neutrophils; VI inhibition of function and proliferation of NK cells; VII inhibition of degranulation of mast cells. cAMP cyclic adenosine monophosphate, CD cluster of differentiation, DCs dendritic cells, IDO indoleamine 2,3-dioxygenase, IL interleukin, mono/mac monocytes/macrophages; NK natural killer, PD-1 programmed cell death-1, Tc cytotoxic T effector, Th T helper
See this image and copyright information in PMC

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