Autoimmune diseases are usually complex and multifactorial, characterized by aberrant production of autoreactive immune cells and/or autoantibodies against healthy cells and tissues. However, the pathogenesis of autoimmune diseases has not been clearly elucidated. The activation, differentiation, and development of CD8+ T cells can be affected by numerous inflammatory cytokines, transcription factors, and chemokines. In recent years, epigenetic modifications have been shown to play an important role in the fate of CD8+ T cells. The discovery of these modifications that contribute to the activation or suppression of CD8+ cells has been concurrent with the increasing evidence that CD8+ T cells play a role in autoimmunity. These relationships have been studied in various autoimmune diseases, including multiple sclerosis (MS), systemic sclerosis (SSc), type 1 diabetes (T1D), Grave's disease (GD), systemic lupus erythematosus (SLE), aplastic anemia (AA), and vitiligo. In each of these diseases, genes that play a role in the proliferation or activation of CD8+ T cells have been found to be affected by epigenetic modifications. Various cytokines, transcription factors, and other regulatory molecules have been found to be differentially methylated in CD8+ T cells in autoimmune diseases. These genes are involved in T cell regulation, including interferons, interleukin (IL),tumor necrosis factor (TNF), as well as linker for activation of T cells (LAT), cytotoxic T-lymphocyte–associated antigen 4 (CTLA4), and adapter proteins. MiRNAs also play a role in the pathogenesis of these diseases and several known miRNAs that are involved in these diseases have also been shown to play a role in CD8+ regulation.

MicroRNA (miRNA)-gene interactions are well-recognized as involved in the progression of almost all cancer types including prostate cancer, which is one of the most common cancers in men. This study explored the significantly dysregulated genes and miRNAs and elucidated the potential miRNA-gene regulatory network in prostate cancer. Integrative analysis of prostate cancer and normal prostate transcriptomic data in The Cancer Genome Atlas dataset was conducted using both differential expression analysis and weighted correlation network analysis (WGCNA). Thirteen genes (RRM2,

Systemic sclerosis (SSc) is a rare autoimmune disease that is characterized by fibrosis, inflammation, and vasculopathy of the skin and internal organs. The etiopathogenesis of SSc remains unclear. However, the pivotal role of T lymphocytes with an aberrant immune response in SSc is well established. Among T cells, IL-17-producing helper T (Th17) cell and regulatory T (Treg) cell subsets have recently been found to play crucial roles in SSc pathogenesis. Generally speaking, Th17 cell subsets up-regulate inflammation, fibrosis, and autoimmunity, which are present in SSc, while Treg cell subsets have an immunosuppressive function and resist the immunological performance of Th17 cells. Up-to-date evidence has pointed out that the imbalance and abnormal functions of Th17/Treg cells may contribute to SSc. Therefore, this review aims to summarize the current understanding of the vital cytokines and signaling pathways that are involved in Th17/Treg differentiation and functions, and their roles in the pathogenesis of SSc, thus providing novel insights about targeting the Th17/Treg balance as a potential therapy for SSc treatment in the near future.