Environmental Triggers and Epigenetics, involved in Autoimmune and Autoinflammatory Disorders

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About this Research Topic

Submission deadlines

  1. Manuscript Summary Submission Deadline 31 January 2025 | Manuscript Submission Deadline 20 April 2025

  2. This Research Topic is still accepting articles.

Background

Environmental triggers such as exposure to air pollution, occupational determinants, smoking habits, alcohol consumption, and dietary habits often have pro-inflammatory effects. These factors are therefore involved in the pathogenesis or exacerbation of autoimmune and autoinflammatory diseases through epigenetic mechanisms, such as DNA methylation, histone modification, or changes in microRNA expression. By their intrinsic function, these mechanisms alter cellular functionality in response to environmental stimuli. In specific contexts of hypersusceptibility, these environmental factors can initiate autoimmune symptoms through the activation of autoinflammatory processes.

The aim of this collection is to highlight the emerging environmental triggers, or even the cumulative effect of multiple triggers, that through epigenetic modifications are implicated in autoimmune pathogenesis, with a focus on the underlying molecular mechanisms linking these factors and on the clinical implication on patients with systemic autoimmune disease.

We invite submissions of various types, including the following:
1. Review Articles: These should provide a comprehensive summary of the current state of research in the field, highlighting existing gaps and outlining future research directions. Reviews should offer an integrated view of the current knowledge and suggest how future investigations should proceed.

2. Original Research Articles: Contributions that provide new evidence—whether epidemiological, observational, or mechanistic/functional—are also of significant interest. These articles should present novel findings that advance understanding in the field and introduce new perspectives or approaches.

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Keywords: Environmental exposure; epigenetics; autoimmune diseases; inflammation

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