FOXP3+ regulatory T cells and their functional regulation

Li, Zhiyuan; Li, Dan; Tsun, Andy; Li, Bin

doi:10.1038/cmi.2015.10

Cited by 238 publications

(183 citation statements)

References 96 publications

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“…Treg functions, especially immunosuppressive functions, are mainly regulated by the expression of the transcription factor FoxP314. Two critical mechanisms have been proposed to explain how stable FoxP3 expression is maintained in Treg; these include interleukin-2 (IL-2) signalling and CNS2 methylation15.…”

mentioning

confidence: 99%

Functional defects in CD4+ CD25high FoxP3+ regulatory cells in ankylosing spondylitis

Guo

Zheng

Zhang

et al. 2016

Sci Rep

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Forkhead box P3 (FoxP3)-positive regulatory T cells (Tregs) play a pivotal role in the preservation of self-tolerance, and Treg dysfunction has been implicated in many autoimmune diseases. Whether and how Tregs participate in the pathogenesis of ankylosing spondylitis (AS) has not been fully elucidated. Here, we investigated Treg function and found that Tregs in peripheral blood (PB) from patients with active AS had lower FoxP3 mean fluorescence intensity (MFI) than those from healthy controls and could not fully suppress naïve T cell (Tn) proliferation. We also studied the mechanisms underlying PB Treg dysfunction in this context and found that PB Tregs failed to effectively utilize IL-2 and had relatively little STAT5 phosphorylation in active AS. Moreover, PB Tregs from patients with active AS exhibited greater CpG island methylation in the CNS2 region of the FOXP3 gene. Therefore, our findings indicate that functional defects in Tregs are present in AS. Abnormal IL-2 signalling and aberrant CNS2 epigenetic control induced functional defects in PB Tregs and represents a potential new mechanism for AS pathogenesis. These findings may aid the design of new treatment approaches for AS.

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mentioning

confidence: 99%

Functional defects in CD4+ CD25high FoxP3+ regulatory cells in ankylosing spondylitis

Guo

Zheng

Zhang

et al. 2016

Sci Rep

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“…Tregs, which are critical for dampening the immune response, have also been shown to secrete cytokines, such as IFNγ, that have important immunoregulatory functions. 28 IFNγ is essential for the induction of FOXP3 in CD4+ T cells. 29, 30 Less research has been conducted on the influence of Tregs on humoral immunity; however, recent studies suggest that Tregs also inhibit B cell responses to antigens through IFNγ-related mechanisms.…”

Section: Discussionmentioning

confidence: 99%

Gene signatures associated with adaptive humoral immunity following seasonal influenza A/H1N1 vaccination

et al. 2016

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This study aimed to identify gene expression markers shared between both influenza hemagglutination-inhibition (HAI) and virus-neutralization antibody (VNA) responses. We enrolled 158 older subjects who received the 2010–2011 trivalent inactivated influenza vaccine (TIV). Influenza-specific HAI and VNA titers, and mRNA-sequencing were performed using blood samples obtained at Days 0, 3 and 28 post-vaccination. For antibody response at Day 28 vs Day 0, several genesets were identified as significant in predictive models for HAI (n=7) and VNA (n=35) responses. Five genesets (comprising the genes MAZ, TTF, GSTM, RABGGTA, SMS, CA, IFNG, and DOPEY) were in common for both HAI and VNA. For response at Day 28 vs Day 3, many genesets were identified in predictive models for HAI (n=13) and VNA (n=41). Ten genesets (comprising biologically related genes, such as MAN1B1, POLL, CEBPG, FOXP3, IL12A, TLR3, TLR7, and others) were shared between HAI and VNA. These identified genesets demonstrated a high degree of network interactions and likelihood for functional relationships. Influenza-specific HAI and VNA responses demonstrated a remarkable degree of similarity. Although unique geneset signatures were identified for each humoral outcome, several genesets were determined to be in common with both HAI and VNA response to influenza vaccine.

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“…Treg cells can be separated according to their two possible origins: tTreg (thymus-derived Treg) cells and pTreg (peripherally derived Treg) cells, also called natural Treg cells and induced Treg cells, respectively (15). Most Treg cells arise in the thymus, where the expression of Foxp3 is initiated via a combination of self-antigen recognition with moderate- to high-avidity and microenvironmental influences, and these tTreg cells migrate to the periphery to maintain self-tolerance (16).…”

Section: Characterization Of Treg Cellsmentioning

confidence: 99%

New Insights into Regulatory T Cells: Exosome- and Non-Coding RNA-Mediated Regulation of Homeostasis and Resident Treg Cells

Liu

et al. 2016

Front. Immunol.

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Regulatory T (Treg) cells are a group of cells that are heterogeneous in origin and in functional activity. Treg cells comprise a necessary balance to adaptive immune responses. As key regulators of self-tolerance, Treg cells have been involved in a series of pathologic processes and considered as therapeutic targets. Here, we summarize recent research regarding Treg cell origins and their functional classification, highlight the role of exosomes and non-coding RNA in modulating Treg cell homeostasis, and discuss the current understanding of resident Treg cells.

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FOXP3+ regulatory T cells and their functional regulation

Cited by 238 publications

References 96 publications

Functional defects in CD4+ CD25high FoxP3+ regulatory cells in ankylosing spondylitis

Functional defects in CD4+ CD25high FoxP3+ regulatory cells in ankylosing spondylitis

Gene signatures associated with adaptive humoral immunity following seasonal influenza A/H1N1 vaccination

New Insights into Regulatory T Cells: Exosome- and Non-Coding RNA-Mediated Regulation of Homeostasis and Resident Treg Cells

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