Abstract
Further observations support the role of environmental factors in autoimmune diseases via the alteration of the epigenetic machinery. In this context, ultraviolet light, smoking, chemicals, and psychological stress have been described as likely examples of this phenomenon. For this study, we took advantage of the PRECISESADS IMI project, which gathered joint data from 2500 individuals with systemic autoimmune diseases, including systemic lupus erythematosus (SLE), systemic sclerosis (SSc), primary Sjögren’s syndrome (pSS), rheumatoid arthritis (RA), primary antiphospholipid syndrome (PAPS), and mixed connective tissue disease (MCTD), and aimed to determine such epigenetic modifications in SLE, SSc, pSS, and RA patients. Here, we performed a set of measures in several countries from the north and south of Europe. We observed that autoimmune patients from the north of Europe presented a higher hypomethylated profile associated with an increased gene expression than patients from the south. These genes were associated with interferon (IFN) pathways, immunity, and the pathways associated with cellular metabolism. Since the IFN scores were increased in this population, these patients presented a more inflammatory profile. To conclude, the geographical location of patients with autoimmune diseases has an impact on DNA methylation, RNA expression, and immunological profiles.
Highlights
The claim was long ago made by the Shoenfeld group that the nature of autoimmune diseases (AIDs), and for a given AID its expression, vary depending on the origin of the patients [1,2,3]
Patients were arbitrary divided into two groups based on their geographic location, and their clinical features are presented in Table 1 and Supplementary Table S1
122 healthy controls (HCs) were from the northern part of Europe, with rheumatoid arthritis (RA) = 174, systemic lupus erythematosus (SLE) = 155, primary Sjögren’s syndrome (pSS) = 108, and
Summary
The claim was long ago made by the Shoenfeld group that the nature of autoimmune diseases (AIDs), and for a given AID its expression, vary depending on the origin of the patients [1,2,3]. It was anticipated that gene involvement, and thereby immune dysfunctions, differ from one country to another. Induced changes have, been shown to modify certain AIDs, giving rise to the key concept of epigenetics. This theory has emerged to explain how cells with a limited number of genes can differentiate into alternative cell types and how a phenotype can be passed from one cell to its daughter cells [4]. Epigenetics can be defined as stable and heritable changes in gene expression that do not involve alterations in DNA sequence. Epigenetic mechanisms are crucial in immune cell differentiation, function, and adaptation to external solicitations
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