Epigenetics of CD4+ T cells in autoimmune diseases

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Abstract

Purpose of review

Autoimmune disorders are a group of overactive symptoms because of abnormal immune responses. Progress of novel mechanisms for autoimmune diseases has been restrained by incomplete understanding of immune disturbance. Recent advances in autoimmune diseases have been well documented by epigenetic alterations (DNA methylation, histone modification, and microRNAs), which alter the transcription activity of genes that are involved in autoimmune responses.

Recent findings

Multiple environmental factors (trichloroethylene, breast milk, and vitamin C) initiate aberrant epigenetic modifications in CD4+ T cells, leading to a list of transcriptional deregulations in several genes (Ifng, Cd70, Tnf, Dnmt3a, and Foxp3) that determine T-cell identity. In addition, epigenetics target regulatory genes (Tim-3, cereblon, protein kinase C theta, octamer transcription factor 1, basic leucine zipper transcription factor ATF-like, p70 kinase, and lactate dehydrogenase A) to influence T-cell activation, differentiation, and metabolism.

Summary

In this review, we decipher findings that identify how epigenetic regulates CD4+ T-cell functions and the advancement of novel epigenetic mechanisms in systemic lupus erythematosus, rheumatoid arthritis, and multiple sclerosis. Further researches could be conducted to explore new clinical application of epigenetic regulation based on T cells in autoimmune diseases.

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