Epigenetics and tissue immunity—Translating environmental cues into functional adaptations*

Tuong, Zewen Kelvin; Stewart, Benjamin J; Guo, Shuang Andrew; Clatworthy, Menna R.

doi:10.1111/imr.13036

Cited by 8 publications

(6 citation statements)

References 307 publications

(330 reference statements)

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“…Continuing technological advances would enable a deeper understanding of the epigenetic mechanisms that control the recruitment, polarization, and activation of immune cells in response to cigarette smoke and allergen co-stimuli at single-cell resolution, and their application in combination with multi-omic strategies to ACO has the potential to identify cell- and tissue-specific epigenetic targets for disease treatments across organs. Integrating all genome and different types of epigenetic alteration data may help to reveal the regulatory role of epigenetics in the formation of ACO more comprehensively [ 90 ]. Clinically, the evaluation and modulation of epigenetics manifest as promising prospects in the diagnosis and treatment of ACO.…”

Section: Discussionmentioning

confidence: 99%

Unraveling the Pathogenesis of Asthma and Chronic Obstructive Pulmonary Disease Overlap: Focusing on Epigenetic Mechanisms

Chen

Chang

Huang

et al. 2022

Cells

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Asthma and COPD overlap (ACO) is characterized by patients presenting with persistent airflow limitation and features of both asthma and COPD. It is associated with a higher frequency and severity of exacerbations, a faster lung function decline, and a higher healthcare cost. Systemic inflammation in COPD and asthma is driven by type 1 T helper (Th1) and Th2 immune responses, respectively, both of which may contribute to airway remodeling in ACO. ACO-related biomarkers can be classified into four categories: neutrophil-mediated inflammation, Th2 cell responses, arachidonic acid-eicosanoids pathway, and metabolites. Gene–environment interactions are key contributors to the complexity of ACO and are regulated by epigenetic mechanisms, including DNA methylation, histone modifications, and non-coding RNAs. Thus, this review focuses on the link between epigenetics and ACO, and outlines the following: (I) inheriting epigenotypes without change with environmental stimuli, or epigenetic changes in response to long-term exposure to inhaled particles plus intermittent exposure to specific allergens; (II) epigenetic markers distinguishing ACO from COPD and asthma; (III) potential epigenetic drugs that can reverse oxidative stress, glucocorticoid insensitivity, and cell injury. Improved understanding of the epigenetic regulations holds great value to give deeper insight into the mechanisms, and clarify their implications for biomedical research in ACO.

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Section: Discussionmentioning

confidence: 99%

Unraveling the Pathogenesis of Asthma and Chronic Obstructive Pulmonary Disease Overlap: Focusing on Epigenetic Mechanisms

Chen

Chang

Huang

et al. 2022

Cells

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“…These interactions influence their epigenetic landscape, allowing for tissue-specific adaptations. 19,122 For example, it has been demonstrated that the gut microbiome influences the epigenetic landscape of ILCs in the small intestine, resulting in phenotypical and functional differences. 123 In support of this hypothesis, Nussbaum et al showed that the effector functions of type 3 ILCs were largely influenced by the tissue of residence and not solely by the tissue of origin.…”

Section: Trafficking and Tissue-residencymentioning

confidence: 99%

“…The development and survival of ILCs require a coordinated interplay between the epithelial and stromal cells of the tissue and the tissue‐resident immune cells. These interactions influence their epigenetic landscape, allowing for tissue‐specific adaptations 19,122 . For example, it has been demonstrated that the gut microbiome influences the epigenetic landscape of ILCs in the small intestine, resulting in phenotypical and functional differences 123 .…”

Section: Nk Cell‐intrinsic Epigenetic Regulation Of Survivalmentioning

confidence: 99%

No time to die: Epigenetic regulation of natural killer cell survival

Hermans,

O'Sullivan

2024

Immunological Reviews

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SummaryNK cells are short‐lived innate lymphocytes that can mediate antigen‐independent responses to infection and cancer. However, studies from the past two decades have shown that NK cells can acquire transcriptional and epigenetic modifications during inflammation that result in increased survival and lifespan. These findings blur the lines between the innate and adaptive arms of the immune system, and suggest that the homeostatic mechanisms that govern the persistence of innate immune cells are malleable. Indeed, recent studies have shown that NK cells undergo continuous and strictly regulated adaptations controlling their survival during development, tissue residency, and following inflammation. In this review, we summarize our current understanding of the critical factors regulating NK cell survival throughout their lifespan, with a specific emphasis on the epigenetic modifications that regulate the survival of NK cells in various contexts. A precise understanding of the molecular mechanisms that govern NK cell survival will be important to enhance therapies for cancer and infectious diseases.

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“…The transmitted epigenetic changes may reflect environmental adaptations made by the parent and transmitted to the offspring through the germline ( 28 , 35 , 180 , 181 ). The offspring of male mice who have been fed a low-protein diet inherit epigenetic marks that affect the peroxisome proliferator-activated receptor alpha (PPARA) gene which regulates lipid and cholesterol metabolism ( 180 ).…”

Section: Transgenerational Inheritance Of Epigenetic Marksmentioning

confidence: 99%

Epigenetic Aspects and Prospects in Autoimmune Hepatitis

Czaja¹

2022

Front. Immunol.

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The observed risk of autoimmune hepatitis exceeds its genetic risk, and epigenetic factors that alter gene expression without changing nucleotide sequence may help explain the disparity. Key objectives of this review are to describe the epigenetic modifications that affect gene expression, discuss how they can affect autoimmune hepatitis, and indicate prospects for improved management. Multiple hypo-methylated genes have been described in the CD4+ and CD19+ T lymphocytes of patients with autoimmune hepatitis, and the circulating micro-ribonucleic acids, miR-21 and miR-122, have correlated with laboratory and histological features of liver inflammation. Both epigenetic agents have also correlated inversely with the stage of liver fibrosis. The reduced hepatic concentration of miR-122 in cirrhosis suggests that its deficiency may de-repress the pro-fibrotic prolyl-4-hydroxylase subunit alpha-1 gene. Conversely, miR-155 is over-expressed in the liver tissue of patients with autoimmune hepatitis, and it may signify active immune-mediated liver injury. Different epigenetic findings have been described in diverse autoimmune and non-autoimmune liver diseases, and these changes may have disease-specificity. They may also be responses to environmental cues or heritable adaptations that distinguish the diseases. Advances in epigenetic editing and methods for blocking micro-ribonucleic acids have improved opportunities to prove causality and develop site-specific, therapeutic interventions. In conclusion, the role of epigenetics in affecting the risk, clinical phenotype, and outcome of autoimmune hepatitis is under-evaluated. Full definition of the epigenome of autoimmune hepatitis promises to enhance understanding of pathogenic mechanisms and satisfy the unmet clinical need to improve therapy for refractory disease.

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Epigenetics and tissue immunity—Translating environmental cues into functional adaptations*

Cited by 8 publications

References 307 publications

Unraveling the Pathogenesis of Asthma and Chronic Obstructive Pulmonary Disease Overlap: Focusing on Epigenetic Mechanisms

Unraveling the Pathogenesis of Asthma and Chronic Obstructive Pulmonary Disease Overlap: Focusing on Epigenetic Mechanisms

No time to die: Epigenetic regulation of natural killer cell survival

Epigenetic Aspects and Prospects in Autoimmune Hepatitis

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