Inflammatory memories: Is epigenetics the missing link to persistent stromal cell activation in rheumatoid arthritis?

Ospelt, Caroline; Reedquist, Kris A.; Gay, Steffen; Tak, Paul P.

doi:10.1016/j.autrev.2011.04.001

Cited by 55 publications

(37 citation statements)

References 59 publications

(61 reference statements)

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“…Histone balance is controlled by different enzymes: histone methyltransferases (HMT) and demethylases (HDM), and histone acetyltransferases (HAT) and deacetylases (HDAC) control the balance of histone modification [94]. HDAC, for example, are the group of enzymes that remove acetyl groups from histone tails that allow condensation of chromatin structures and the repression of gene expression [95]. In some cases such as RA [96], the correlation of specific histone modifications and gene expression associated with AIDs has been well investigated.…”

Section: Histone Post-translational Modificationmentioning

confidence: 99%

The epigenetics of PBC: The link between genetic susceptibility and environment

Marzorati

Lleo

Carbone

et al. 2016

Clinics and Research in Hepatology and Gastroenterology

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Section: Histone Post-translational Modificationmentioning

confidence: 99%

The epigenetics of PBC: The link between genetic susceptibility and environment

Marzorati

Lleo

Carbone

et al. 2016

Clinics and Research in Hepatology and Gastroenterology

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“…Epigenetic reduction of histone deactylase 2 and its activity has been connected to oxidative stress, lung inflammation and increased risk of chronic obstructive pulmonary disease (COPD) [116]. Ospelt et al [117] proposed that epigenetically produced inflammatory memory may be the key to risk of rheumatoid arthritis (RA). These authors suggested that a stable activation of synovial fibroblasts may provide the key step leading to improper inflammation and RA.…”

Section: Altered Epigenetic Programming (Aep) Across Generationsmentioning

confidence: 99%

The Completed Self: An Immunological View of the Human-Microbiome Superorganism and Risk of Chronic Diseases

Dietert

Dietert²

2012

Entropy

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Abstract:In this review, we discuss an immunological-driven sign termed the Completed Self, which is related to a holistic determination of health vs. disease. This sign (human plus commensal microbiota) forms the human superorganism. The worldwide emergence of an epidemic of chronic diseases has caused increased healthcare costs, increased premature mortality and reduced quality of life for a majority of the world's population. In addition, it has raised questions concerning the interactions between humans and their environment and potential imbalances. Misregulated inflammation, a host defensehomeostasis disorder, appears to be a key biomarker connecting a majority of chronic diseases. We consider the apparent contributors to this disorder that promote a web of interlinked comorbid conditions. Three key events are suggested to play a role: (1) altered epigenetic programming (AEP) that may span multiple generations, (2) developmental immunotoxicity (DIT), and (3) failure to adequately incorporate commensal microbes as a newborn (i.e., the incomplete self). We discuss how these three events can combine to determine whether the human superorganism is able to adequately and completely form during early childhood. We also discuss how corruption of this event can affect the risk of later-life diseases.

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“…SSc [115][116][117] and rheumatoid arthritis (RA) [118,119] represent conditions in which environmental factors have different weights [120,121], as well illustrated by the significantly different concordance rates in monozygotic twins which are below 5% and lower compared to dizygotic twins [31] and approximately 15%, respectively (Table 1). For these reasons, one would expect different roles of epigenetic changes as well but data from disease-specific fibroblasts share some common features [120,122].…”

Section: From Geoepidemiology To Pollution In Slementioning

confidence: 99%

The Therapeutic Potential of Epigenetics in Autoimmune Diseases

Santis

Selmi

2011

Clinic Rev Allerg Immunol

109

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A variety of mechanisms have been suggested as the means by which infections can initiate and/or exacerbate autoimmune diseases. One mechanism is molecular mimicry, where a foreign antigen shares sequence or structural similarities with self-antigens. Molecular mimicry has typically been characterized on an antibody or T cell level. However, structural relatedness between pathogen and self does not account for T cell activation in a number of autoimmune diseases. A proposed mechanism that could have been misinterpreted for molecular mimicry is the expression of dual T cell receptors (TCR) on a single T cell. These T cells have dual reactivity to both foreign and self-antigens leaving the host vulnerable to foreign insults capable of triggering an autoimmune response. In this review, we briefly discuss what is known about molecular mimicry followed by a discussion of the current understanding of dual TCRs. Finally, we discuss three mechanisms, including molecular mimicry, dual TCRs and chimeric TCRs, by which dual reactivity of the T cell may play a role in autoimmune diseases.

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Inflammatory memories: Is epigenetics the missing link to persistent stromal cell activation in rheumatoid arthritis?

Cited by 55 publications

References 59 publications

The epigenetics of PBC: The link between genetic susceptibility and environment

The epigenetics of PBC: The link between genetic susceptibility and environment

The Completed Self: An Immunological View of the Human-Microbiome Superorganism and Risk of Chronic Diseases

The Therapeutic Potential of Epigenetics in Autoimmune Diseases

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