Abstract
The molecular mechanisms of inflammation involve a series of processes that start as extracellular signals that interact with membrane-bound receptors, cell signaling cascades, nuclear factors, and epigenetic enzymes that activate a specific gene expression program. Environmental factors and/or genetic defects can result in constitutive activation of this program. Recent studies highlight the relevance of epigenetic (dys)regulation in these processes and suggest several implications of these mechanisms and alterations in the clinical management of patients with autoinflammatory diseases. In this chapter, we provide an overview of the latest findings related to the epigenetic control in the function of myeloid cells as main effectors of inflammation, as well as the latest findings in the field of autoinflammatory diseases.
Keywords
Autoinflammation Epigenetics DNA methylation Myeloid cellsAbbreviations
- 5hmC
5-hydroxymethylcytosine
- 5mC
5-methylcytosine
- AID
Activation-induced cytidine deaminase
- AIM2
Absent in melanoma 2
- AP-1
Activator protein
- ASC
Apoptosis-associated speck-like protein
- C/EBPα
CCAAT/enhancer binding protein
- CAPS
Cryopyrin-associated periodic syndromes
- CD
Crohn disease
- CNO
Chronic non-bacterial osteomyelitis
- CREB
cAMP response element-binding protein
- DAMPs
Danger-associated molecular patterns
- DNMTs
DNA methyltransferases
- EBF1
Early B cell factor 1
- ETS
E26 transformation-specific
- FCAS
Familial cold autoinflammatory syndrome
- FMF
Familial Mediterranean fever
- HATs
Histone acetyltransferases
- HDACs
Histone deacetylases
- HIDS
Hyperimmunoglobulinemia D syndrome
- HMTs
Histone methyltransferases
- HSCs
Hematopoietic stem cells
- IKKs
IκB kinases
- IL
Interleukin
- IRAK
Interleukin-1 receptor-associated kinases
- IRF
Interferon-regulatory factors
- I-SRE
Intronic enhancer element
- JmjC
Jumonji domain-containing proteins
- JNK
c-Jun N-terminal kinases
- LPS
Lipopolysaccharide
- MAPKs
Mitogen-activated protein kinases
- MKD
Mevalonate kinase deficiency
- MWS
Muckle-Wells syndrome
- NLR
NOD-like receptor
- NOMID
Neonatal-onset multisystem inflammatory disease
- PAMPs
Pathogen-associated molecular patterns
- PAX5
Paired box protein 5
- PGE2
Prostaglandin E2
- PRRs
Pattern-recognition receptors
- STAT
Signal transducer and activator of transcription
- TET
Ten-eleven translocation
- TNF
Tumor necrosis factor
- TRAF
Tumor necrosis factor receptor-associated factor
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