Intestinal Regulatory T Cells

Paz, Vanessa Ribeiro Figliuolo da; Jamwal, Deepa R.; Kiela, Pawel R.

doi:10.1007/978-981-15-6407-9_9

Cited by 12 publications

(8 citation statements)

References 392 publications

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Section: Resultsmentioning

confidence: 99%

“…Deficiency in Tregs stability, function, and generation in the gut causes inflammation and increases the risk of CAC [20]. Intestinal Tregs can produce high levels of inhibitory cytokines to suppress intestinal immune responses and maintain intestinal homeostasis [20]. To determine the effect of STAT6 deficiency on intestinal Tregs generation and stability during carcinogenesis in our model, we examined the frequency of Tregs in the colon of WT Foxp3 EGFP AOM and STAT6‐/‐Foxp3 EGFP AOM mice during the early stage of tumor development (Fig.…”

Section: Resultsmentioning

confidence: 99%

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STAT6 controls the stability and suppressive function of regulatory T cells

et al. 2023

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Signal transducer and activator of transcription 6 (STAT6) promotes tumorigenesis by decreasing the Forkhead box P3+ (Foxp3+) cell frequency allowing for the infiltration of inflammatory cells during the early stages of colitis‐associated cancer (CAC). In this study, we dissected the role of STAT6 in the generation of inducible in vitro regulatory T cells (iTregs) and peripheral in vivo Tregs (pTregs) under inflammatory conditions. In in vitro assays, when STAT6 was lacking, iTregs preserved a stable phenotype and expressed high levels of Foxp3 and CD25 during long expansion periods, even in the presence of IL‐6. This effect was associated with increased in vitro suppressive ability, over‐expression of programmed death‐1 (PD‐1), CTLA‐4, and Foxp3, and decreased IFN‐γ expression. Furthermore, iTregs developed during STAT6 deficiency showed a higher demethylation status for the FOXP3 Treg‐specific demethylated region (TSDR), coupled with lower DNA methyltransferase 1 (DNMT1) mRNA expression, suggesting that STAT6 may lead to Foxp3 silencing. Using a mouse model of CAC, the STAT6‐/‐ pTregs expressed a more activated phenotype at the intestine, had higher suppressive capacity, and expressed more significant levels of PD‐1 and latency‐associated peptide of TGF‐β (LAP) associated with their ability to attenuate tumor development. These data suggest that STAT6 signaling impairs the induction, stability, and suppressive capacity of Tregs developed in vitro or in vivo during gut inflammation.

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Section: Resultsmentioning

confidence: 99%

Section: Resultsmentioning

confidence: 99%

STAT6 controls the stability and suppressive function of regulatory T cells

et al. 2023

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“…SCFAs can also regulate the adaptive immune system; for example, they can affect the differentiation of regulatory T cells (Treg) ( Veltkamp et al, 2006 ; Fang et al, 2021 ). Treg cells, marked by the expression of the FOXP3 transcription factor, play an important role in suppressing unwanted immune responses and maintaining homeostasis ( Moes et al, 2010 ; Figliuolo da Paz et al, 2021 ). The differentiation, maintenance, and migration of Treg cells are regulated by various signals provided by the microbiota ( Wang et al, 2018 ).…”

Section: Potential Mechanism Of the Mgba In Preterm Infants With Wmimentioning

confidence: 99%

Pathogenesis from the microbial-gut-brain axis in white matter injury in preterm infants: A review

Wang

Zhu

Zhang

et al. 2023

Front. Integr. Neurosci.

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White matter injury (WMI) in premature infants is a unique form of brain injury and a common cause of chronic nervous system conditions such as cerebral palsy and neurobehavioral disorders. Very preterm infants who survive are at high risk of WMI. With developing research regarding the pathogenesis of premature WMI, the role of gut microbiota has attracted increasing attention in this field. As premature infants are a special group, early microbial colonization of the microbiome can affect brain development, and microbiome optimization can improve outcomes regarding nervous system development. As an important communication medium between the gut and the nervous system, intestinal microbes form a microbial-gut-brain axis. This axis affects the occurrence of WMI in premature infants via the metabolites produced by intestinal microorganisms, while also regulating cytokines and mediating oxidative stress. At the same time, deficiencies in the microbiota and their metabolites may exacerbate WMI in premature infants. This confers promise for probiotics and prebiotics as treatments for improving neurodevelopmental outcomes. Therefore, this review attempted to elucidate the potential mechanisms behind the communication of gut bacteria and the immature brain through the gut-brain axis, so as to provide a reference for further prevention and treatment of premature WMI.

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“…133 Treg cell-derived exosomes can promote IEC proliferation, inhibit IEC apoptosis, and protect the intestinal barrier in IBD mouse model. 134,135 Granulocytic myeloid-derived exosomes can alleviate IBD by diminishing the proportion of Th1 cells, and promoting the expansion of Treg cells. 136 These immune cell-derived exosomes may be the new therapeutic intervention for IBD in the future.…”

Section: Dovepressmentioning

confidence: 99%

Extracellular Vesicles: The Next Generation Theranostic Nanomedicine for Inflammatory Bowel Disease

Li¹,

Yang²,

Xu³

et al. 2022

IJN

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The recent rapid development in the field of extracellular vesicles (EVs) based nanotechnology has provided unprecedented opportunities for nanomedicine platforms. As natural nanocarriers, EVs such as exosomes, exosome-like nanoparticles and outer membrane vesicles (OMVs), have unique structure/composition/morphology characteristics, and show excellent physical and chemical/biochemical properties, making them a new generation of theranostic nanomedicine. Here, we reviewed the characteristics of EVs from the perspective of their formation and biological function in inflammatory bowel disease (IBD). Moreover, EVs can crucially participate in the interaction and communication of intestinal epithelial cells (IECs)-immune cells-gut microbiota to regulate immune response, intestinal inflammation and intestinal homeostasis. Interestingly, based on current representative examples in the field of exosomes and exosome-like nanoparticles for IBD treatment, it is shown that plant, milk, and cells-derived exosomes and exosomelike nanoparticles can exert a therapeutic effect through their components, such as proteins, nucleic acid, and lipids. Moreover, several drug loading methods and target modification of exosomes are used to improve their therapeutic capability. We also discussed the application of exosomes and exosome-like nanoparticles in the treatment of IBD. In this review, we aim to better and more clearly clarify the underlying mechanisms of the EVs in the pathogenesis of IBD, and provide directions of exosomes and exosome-like nanoparticles mediated for IBD treatment.

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Intestinal Regulatory T Cells

Cited by 12 publications

References 392 publications

STAT6 controls the stability and suppressive function of regulatory T cells

STAT6 controls the stability and suppressive function of regulatory T cells

Pathogenesis from the microbial-gut-brain axis in white matter injury in preterm infants: A review

Extracellular Vesicles: The Next Generation Theranostic Nanomedicine for Inflammatory Bowel Disease

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