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Cells
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From Epigenetics and 3D Chromatin in Immune Cells to Therapeutics...
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From Epigenetics and 3D Chromatin in Immune Cells to Therapeutics of Autoimmune Diseases

A special issue of Cells (ISSN 2073-4409). This special issue belongs to the section "Cellular Immunology".

Deadline for manuscript submissions: closed (20 May 2022) | Viewed by 7109

Special Issue Editors

Dr. Gangqing (Michael) Hu

E-Mail Website
Guest Editor
Department of Microbiology, Immunology, and Cell Biology, West Virginia University, Morgantown, WV 26506-9177, USA
Interests: NGS; genomics; cancer epigenomics; T cells; 3D genome; single-cell omics; data Integration
Dr. Peng Li

grade E-Mail Website
Guest Editor
National Heart, Lung and Blood Institute, National Institutes of Health, Bethesda, MD 20892, USA
Interests: molecular and cellular immunology; chromatin remodeling; cytokine regulation; gene expression and regulation
Dr. Chao Zhong

E-Mail Website
Guest Editor
Institute of Systems Biomedicine, School of Basic Medical Sciences, Peking University Health Science Center, Beijing 100191, China
Interests: immunology; transcription factor; epigenetics; metabolism

Special Issue Information

Dear Colleagues,

Autoimmune diseases are caused by the abnormal expression of disease-causal genes, non-coding RNAs, and genetic variants in immune cells. Epigenetic regulation alters molecular and cellular functions by modulating transcription programs without genetic mutations. DNA methylation, histone modifications, and non-coding RNA are among the main epigenetic events. In addition to genetic mutations, the pathophysiology of autoimmune diseases is strongly associated with epigenetic dysregulation in coping with external stimuli, such as viral infection and environmental stress. Regulatory elements can also modulate the expression of disease-causal genes via long-distance chromatin interactions with an alternation in the interactions linked to diseases including autoimmune disease. Epigenetic regulation in the 3D chromatin of immune cells is an emerging and fast-moving field, which casts new insights into the causal mechanisms of autoimmune disease with implications in novel therapeutics.

This Special Issue invites topics related to various epigenetic events, including 3D chromatin, in immune cells. It provides an update on our knowledge of the underlying molecular mechanisms, including epigenetic contributions and the role of chromatin conformation to autoimmune disorders. The issue also welcomes submissions that provide insights into novel approaches for predicting disease progression and outcome, as well as the design of targeted, cost-effective, new epigenetic therapies for autoimmune diseases.

Dr. Gangqing (Michael) Hu
Dr. Peng Li
Dr. Chao Zhong
Guest Editors

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Cells is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2700 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • gene regulation
  • epigenetics
  • 3D chromatin
  • histone modification
  • chromatin regulators
  • autoimmune disease
  • therapeutics

Published Papers (2 papers)

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25 pages, 2135 KiB  
Review
Abnormal Epigenetic Regulations in the Immunocytes of Sjögren’s Syndrome Patients and Therapeutic Potentials
by Peng Li, Mengwei Han, Xingyu Zhao, Guanqun Ren, Si Mei and Chao Zhong
Cells 2022, 11(11), 1767; https://doi.org/10.3390/cells11111767 - 27 May 2022
Cited by 6 | Viewed by 2955
Abstract
Sjögren’s syndrome (SjS), characterized by keratoconjunctivitis sicca and dry mouth, is a common autoimmune disease, especially in middle-aged women. The immunopathogenesis of SjS is caused by the sequential infiltration of T and B cells into exocrine glands, including salivary and lacrimal glands. Effector [...] Read more.
Sjögren’s syndrome (SjS), characterized by keratoconjunctivitis sicca and dry mouth, is a common autoimmune disease, especially in middle-aged women. The immunopathogenesis of SjS is caused by the sequential infiltration of T and B cells into exocrine glands, including salivary and lacrimal glands. Effector cytokines produced by these immunocytes, such as interferons (IFNs), IL-17, IL-22, IL-21, IL-4, TNF-α, BAFF and APRIL, play critical roles in promoting autoimmune responses and inducing tissue damages. Epigenetic regulations, including DNA methylation, histone modification and non-coding RNAs, have recently been comprehensively studied during the activation of various immunocytes. The deficiency of key epigenetic enzymes usually leads to aberrant immune activation. Epigenetic modifications in T and B cells are usually found to be altered during the immunopathogenesis of SjS, and they are closely correlated with autoimmune responses. In particular, the important role of methylation in activating IFN pathways during SjS progression has been revealed. Thus, according to the involvement of epigenetic regulations in SjS, target therapies to reverse the altered epigenetic modifications in auto-responsive T and B cells are worthy of being considered as a potential therapeutic strategy for SjS. Full article
(This article belongs to the Special Issue From Epigenetics and 3D Chromatin in Immune Cells to Therapeutics of Autoimmune Diseases)
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7 pages, 264 KiB  
Review
Epigenetic Alterations in Immune Cells of Systemic Lupus Erythematosus and Therapeutic Implications
by David E. Adams and Wen-Hai Shao
Cells 2022, 11(3), 506; https://doi.org/10.3390/cells11030506 - 01 Feb 2022
Cited by 15 | Viewed by 3523
Abstract
Systemic lupus erythematosus (SLE) is an autoimmune disorder that is characterized by autoantibody production and dysregulated immune cell activation. Although the exact etiology of SLE remains unknown, genetic, hormonal, and complex environmental factors are known to be critical for pathologic immune activation. In [...] Read more.
Systemic lupus erythematosus (SLE) is an autoimmune disorder that is characterized by autoantibody production and dysregulated immune cell activation. Although the exact etiology of SLE remains unknown, genetic, hormonal, and complex environmental factors are known to be critical for pathologic immune activation. In addition to the inherited genetic predisposition, epigenetic processes that do not change the genomic code, such as DNA methylation, histone modification, and noncoding RNAs are increasingly appreciated to play important roles in lupus pathogenesis. We herein focus on the up-to-date findings of lupus-associated epigenetic alterations and their pathophysiology in lupus development. We also summarize the therapeutic potential of the new findings. It is likely that advances in the epigenetic study will help to predict individual disease outcomes, promise diagnostic accuracy, and design new target-directed immunotherapies. Full article
(This article belongs to the Special Issue From Epigenetics and 3D Chromatin in Immune Cells to Therapeutics of Autoimmune Diseases)
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