Regulatory T Cells: Concept, Classification, Phenotype, and Biological Characteristics

Du, Yang; Fang, Qiannan; Zheng, Simin

doi:10.1007/978-981-15-6407-9_1

Cited by 11 publications

(11 citation statements)

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“…Treg cells are mainly recognized for their suppressive function that keep excessive inflammatory responses under control, although emerging data suggest additional roles of Treg cells in non-immune settings during tissue regeneration, such as in stimulating hair follicle ( 7 ) and muscle repair ( 8 ). Since the initial identification of FOXP3 as a Treg master transcription factor ( 9 – 13 ), the discovery of additional types of regulatory T cells has continued ( 14 ). In humans, FOXP3 is also expressed in activated effector conventional T cells (Tcon) without any associated suppressive activities ( 15 – 17 ); however, in mice, Foxp3 is still considered as the exclusive master transcription factor of Treg cells ( 18 ).…”

Section: Introductionmentioning

confidence: 99%

Treg-specific deletion of the phosphatase SHP-1 impairs control of inflammation in vivo

Tung

Lorenz

2023

Front. Immunol.

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IntroductionTo achieve a healthy and functional immune system, a delicate balance exists between the activation of conventional T cells (Tcon cells) and the suppression by regulatory T cells (Treg). The tyrosine phosphatase SHP-1, a negative regulator of TCR signaling, shapes this ‘activation-suppression’ balance by modulating Tcon cell resistance to Treg-mediated suppression. Treg cells also express SHP-1, but its role in influencing Treg function is still not fully understood. MethodsWe generated a Treg-specific SHP-1 deletion model, Foxp3Cre+ Shp-1f/f, to address how SHP-1 affects Treg function and thereby contributes to T cell homeostasis using a combination of ex vivo studies and in vivo models of inflammation and autoimmunity.ResultsWe show that SHP-1 modulates Treg suppressive function at different levels. First, at the intracellular signaling level in Treg cells, SHP-1 attenuates TCR-dependent Akt phosphorylation, with loss of SHP-1 driving Treg cells towards a glycolysis pathway. At the functional level, SHP-1 expression limits the in vivo accumulation of CD44hiCD62Llo T cells within the steady state Tcon populations (both CD8+ as well as CD4+ Tcon). Further, SHP-1-deficient Treg cells are less efficient in suppressing inflammation in vivo; mechanistically, this appears to be due to a failure to survive or a defect in migration of SHP-1-deficient Treg cells to peripheral inflammation sites.ConclusionOur data identify SHP-1 as an important intracellular mediator for fine-tuning the balance between Treg-mediated suppression and Tcon activation/resistance.

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Section: Introductionmentioning

confidence: 99%

Treg-specific deletion of the phosphatase SHP-1 impairs control of inflammation in vivo

Tung

Lorenz

2023

Front. Immunol.

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“…Tr1 Treg cells mainly produce interleukin (IL)-10, while Th3 cells primarily secrete transforming growth factor beta (TGF-β). 4 , 37 …”

Section: Classification Of Treg Cellsmentioning

confidence: 99%

Beyond Immune Balance: The Pivotal Role of Decidual Regulatory T Cells in Unexplained Recurrent Spontaneous Abortion

Li,

Zhao,

Yang

et al. 2024

JIR

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Recurrent spontaneous abortion (RSA) is defined as two or more consecutive pregnancy failures, which brings tremendous stress to women of childbearing age and seriously affects family well-being. However, the reason in about 50% of cases remains unknown and is defined as unexplained recurrent spontaneous abortion (URSA). The immunological perspective in URSA has attracted widespread attention in recent years. The embryo is regarded as a semi-allogeneic graft to the mother. A successful pregnancy requires transition to an immune environment conducive to embryo survival at the maternal–fetal interface. As an important member of regulatory immunity, regulatory T (Treg) cells play a key role in regulating immune tolerance at the maternal–fetal interface. This review will focus on the phenotypic plasticity and lineage stability of Treg cells to illustrate its relationship with URSA.

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“…A heightened immune response, caused by abnormal regulation of T helper and Tregs and increased IgE production, consequently leading to atopic diseases, is common in DOCK8 deficient patients ( Aydin et al, 2015 ). This may partly be due to the significant numerical reduction of Tregs ( Caracciolo et al, 2014 ; Du et al, 2021 ). Tregs, a subset of CD4 + T cells, provide an essential negative immunomodulatory function in immune homeostasis and maintaining immune tolerance towards self-antigens ( Singh et al, 2017 ).…”

Section: The Role Of Dock8mentioning

confidence: 99%

“…Tregs, a subset of CD4 + T cells, provide an essential negative immunomodulatory function in immune homeostasis and maintaining immune tolerance towards self-antigens ( Singh et al, 2017 ). In the absence of DOCK8, the capacity of Tregs to suppress the proliferation of T cells is absent causing autoimmunity ( Shi et al, 2018 ; Du et al, 2021 ). This may be attributed to an impaired function of the role of DOCK8 in IL-2 signalling ( Randall et al, 2011 ; Shi et al, 2018 ), impaired Treg migration ( Randall et al, 2021 ), and defective thymocyte differentiation to Treg ( Janssen et al, 2021 ).…”

Section: The Role Of Dock8mentioning

confidence: 99%

“…This may be attributed to an impaired function of the role of DOCK8 in IL-2 signalling ( Randall et al, 2011 ; Shi et al, 2018 ), impaired Treg migration ( Randall et al, 2021 ), and defective thymocyte differentiation to Treg ( Janssen et al, 2021 ). Susceptibility towards atopic diseases may in addition be caused by the bias towards Th2 ( Engelhardt et al, 2015 ), lack of peripheral B cell tolerance, and increases in autoantibody production ( Du et al, 2021 ).…”

Section: The Role Of Dock8mentioning

confidence: 99%

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CRISPR/Cas-Based Gene Editing Strategies for DOCK8 Immunodeficiency Syndrome

et al. 2022

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Defects in the DOCK8 gene causes combined immunodeficiency termed DOCK8 immunodeficiency syndrome (DIDS). DIDS previously belonged to the disease category of autosomal recessive hyper IgE syndrome (AR-HIES) but is now classified as a combined immunodeficiency (CID). This genetic disorder induces early onset of susceptibility to severe recurrent viral and bacterial infections, atopic diseases and malignancy resulting in high morbidity and mortality. This pathological state arises from impairment of actin polymerization and cytoskeletal rearrangement, which induces improper immune cell migration-, survival-, and effector functions. Owing to the severity of the disease, early allogenic hematopoietic stem cell transplantation is recommended even though it is associated with risk of unintended adverse effects, the need for compatible donors, and high expenses. So far, no alternative therapies have been developed, but the monogenic recessive nature of the disease suggests that gene therapy may be applied. The advent of the CRISPR/Cas gene editing system heralds a new era of possibilities in precision gene therapy, and positive results from clinical trials have already suggested that the tool may provide definitive cures for several genetic disorders. Here, we discuss the potential application of different CRISPR/Cas-mediated genetic therapies to correct the DOCK8 gene. Our findings encourage the pursuit of CRISPR/Cas-based gene editing approaches, which may constitute more precise, affordable, and low-risk definitive treatment options for DOCK8 deficiency.

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Regulatory T Cells: Concept, Classification, Phenotype, and Biological Characteristics

Cited by 11 publications

References 274 publications

Treg-specific deletion of the phosphatase SHP-1 impairs control of inflammation in vivo

Treg-specific deletion of the phosphatase SHP-1 impairs control of inflammation in vivo

Beyond Immune Balance: The Pivotal Role of Decidual Regulatory T Cells in Unexplained Recurrent Spontaneous Abortion

CRISPR/Cas-Based Gene Editing Strategies for DOCK8 Immunodeficiency Syndrome

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