Abstract
Environmental factors contribute to autoimmune disease manifestation, and as regarded today, AhR has become an important factor in studies of immunomodulation. Besides immunological aspects, AhR also plays a role in pharmacological, toxicological and many other physiological processes such as adaptive metabolism. In recent years, epigenetic mechanisms have provided new insight into gene regulation and reveal a new contribution to autoimmune disease pathogenesis. DNA methylation, histone modifications, chromatin alterations, microRNA and consequently non-genetic changes in phenotypes connect with environmental factors. Increasing data reveals AhR cross-roads with the most significant in immunology pathways. Although study on epigenetic modulations in autoimmune diseases is still not well understood, therefore future research will help us understand their pathophysiology and help to find new therapeutic strategies. Present literature review sheds the light on the common ground between remodeling chromatin compounds and autoimmune antibodies used in diagnostics. In the proposed review we summarize recent findings that describe epigenetic factors which regulate AhR activity and impact diverse immunological responses and pathological changes.
Highlights
Heredity is only the sum of all past environment—this famous statement published in 1906 in the article “The Training of the Human Plant” in Century magazine by Luther Burbank [1] has never been so much reliable and evident as in recent years when epigenetics and its underlying mechanisms have changed classical approach to many topics requiring a thorough understanding of all aspects of genetics, such as stem cells, cloning, aging or synthetic biology [2]
aryl hydrocarbon receptor (AhR) regulates the differentiation of Th17 and Treg cells; the difference in its expression shifts the balance between these two T cell subtypes and may contribute to the pathogenesis, among others, of Crohn’s diseases (CD)
Based on the above literature, we can see that it may be implicated into epigenetic processes which are significant in immunomodulation
Summary
Heredity is only the sum of all past environment—this famous statement published in 1906 in the article “The Training of the Human Plant” in Century magazine by Luther Burbank [1] has never been so much reliable and evident as in recent years when epigenetics and its underlying mechanisms have changed classical approach to many topics requiring a thorough understanding of all aspects of genetics, such as stem cells, cloning, aging or synthetic biology [2]. In the case of those kinds of pathological conditions well-established heritability model is problematic and very often it is a subject of controversy [5] In this respect, more in-depth research providing epigenetic studies could be a great value in searching for potential biomarkers, molecular mechanisms responsible for maintaining balance in autoimmunity, and crucial in clinical aspects such as efficient drug therapy. Shinde et al [21] revealed that AhR is activated by TLR9 and DNA from apoptotic cells in systemic lupus erythematosus patients (SLE) [21]. This assumption that TLR ligands and cytokines are potent agonists in various cell types has been pointed even a few years back by other authors [22,23]. ANA, antinuclear antibodies; ANCA, antineutrophil cytoplasmic antibodies; ACPA, anticitrullinated protein. antibodies; β2GPI, β2 glycoprotein 1; CL, cardiolipin; LA, lupus anticoagulants; RF, rheumatoid factor; RNP, ribonucleoprotein; ↑, upregulation (increased); ↓, downregulation (decreased); ?, unknown association
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