Editorial: Epigenetic aspects of autoimmune diseases

• Published in: Frontiers in cell and developmental biology 2022-08, Vol.10, p.991693-991693
• Main Authors: Brooks, Wesley H., Arleevskaya, Marina I., Renaudineau, Yves
• Format: Article
• Language: English
• Subjects: Cell and Developmental Biology; epigenetics; Human health and pathology; Life Sciences; lupus (SLE); multiple sclerosis; rheumatoid arthritis; sjogren’s syndrome
• ISSN: 2296-634X; 2296-634X
• DOI: 10.3389/fcell.2022.991693

Genetics, environmental factors, and epigenetics all contribute to autoimmune disease onset and progression (Gulati and Brunner, 2018). Most of the earlier research on autoimmune diseases focused on genetics and environmental factors. Research into genetics, in attempting to identify specific risk alleles has had limited success, for example, identifying HLA-DRB1, a complex of genes coding for cell surface proteins, has emerged as a risk allele for autoimmune diseases such as systemic lupus erythematosus (SLE) and rheumatoid arthritis (RA) (Niu et al., 2015). However, genetic findings have not been sufficient to explain the majority of RA and SLE cases, autoimmune diseases in general, or the typical delay in initial onset, occurring later in life (early to mid-adulthood), in most autoimmune diseases. Even with identification of a risk allele, it is not clear if it is a cause of the disease or just a subsidiary factor. Likewise, environmental factors (e.g., viruses, toxins, bacteria, etc.) also present confusion as to their role since a variety of environmental factors and combinations can be involved in triggering onset of an autoimmune disease (Arleevskaya et al., 2016; Arleevskaya et al., 2020). For example, Epstein-Barr virus (EBV) is suspected of a role in autoimmune diseases, especially multiple sclerosis (MS) (Bjornevik et al., 2022). However, almost all adults have had exposure to EBV but only a small percentage develop MS and onset can be many years after initial infection with EBV. It may be that another environmental factor and/or a genetic risk allele needs to be involved, such as an especially heavy cellular viral load of EBV that may occur by viral binding and entry using HLA-DR cell surface proteins as opposed to other HLA types (Agostini et al., 2018). Research into the involvement of epigenetics in autoimmune diseases has been steadily increasing in the past two decades. Epigenetics is the control of gene expression or suppression without changing the underlying DNA sequence of the gene (Renaudineau et al., 2011). Epigenetics can involve methylation of DNA, which typically suppresses the underlying gene, or demethylation of the DNA as a step towards expression (Fali et al., 2014). Coordinated with the DNA methylation state are