Abstract
As the most prevalent internal modification in mRNA, N (6)-methyladenosine (m(6)A) plays broad biological functions via fine-tuning gene expression at the post-transcription level. Such modifications are deposited by methyltransferases (i.e., m(6)A Writers), removed by demethylases (i.e., m(6)A Erasers), and recognized by m(6)A binding proteins (i.e., m(6)A Readers). The m(6)A decorations regulate the stability, splicing, translocation, and translation efficiency of mRNAs, and exert crucial effects on proliferation, differentiation, and immunologic functions of immunocytes, such as T lymphocyte, B lymphocyte, dendritic cell (DC), and macrophage. Recent studies have revealed the association of dysregulated m(6)A modification machinery with various types of diseases, including AIDS, cancer, autoimmune disease, and atherosclerosis. Given the crucial roles of m(6)A modification in activating immunocytes and promoting DNA repair in cells under physiological or pathological states, targeting dysregulated m(6)A machinery holds therapeutic potential in clinical application. Here, we summarize the biological functions of m(6)A machinery in immunocytes and the potential clinical applications via targeting m(6)A machinery.