N6-methyladenosine (m6A) is the most abundant modification on mRNA and lncRNA. Numerous studies have shown that m6A modifications play important roles in RNA metabolisms, such as stability, translation, transportation, and localization. It has been recognized that m6A-related proteins, including methyltransferase (METTL3, METTL14, METTL16), demethylases (FTO, ALKBH5), ‘reader’ proteins (YTHDF1/2/3, YTHDC1/2, IGF2BP1/2/3), and other cooperated proteins that involved in m6A machinery, regulate normal tissue development and disease pathogenesis.
The immune system, which comprises innate immunity and adaptive immunity, protects our body from outside invaders. Innate immune cells include myeloid cells (macrophages, neutrophils, eosinophils, basophils, MDSCs, and dendritic cells), innate lymphoid cells (NK cells, ILC1, ILC2, ILC3, and LTi cells), ?d T cells, NKT cells, and mast cells. The adaptive immune system includes antigen-specific T cells, which are activated to proliferate through the action of APCs, and B cells which differentiate into plasma cells to produce antibodies.
RNA-mediated epigenetic regulation of cell functions and development is becoming more and more attractive. m6A modification is required for many processes in immune cells, including development, differentiation, activation, and polarization, thereby modulating the immune response. Our topic will mainly focus on the following aspects:
1. How m6A modifications regulate immune cell development, differentiation, or polarization. For example, the development of myeloid cells (macrophages, neutrophils, eosinophils, basophils, MDSCs, and dendritic cells), ?d T cells, NKT cells, and innate lymphoid cells (NK cells, ILC1, ILC2, ILC3, and LTi cells). T cell lineage (precursor T, memory T, etc.), and B cell lineage (progenitor B, precursor B, immature B, mature B, memory B).
2. Regulation of m6A machinery in immune cell-related diseases and neoplasms, for example, tumor or tumor microenvironment related/infiltrated immune cells, immune-related myeloid cells, tumor-infiltrated myeloid and lymphoid cells, immunosuppressive myeloid-derived suppressor cells, immunodeficiencies, autoimmune disease, hypersensitivity, idiopathic inflammation, B-cell leukemia (pre-B ALL), lymphoma (CLL, BCDCL, MCL, etc.), T-cell disease, T-cell leukemia, etc.
We are aiming to contribute to the basic studies of the full landscape of RNA epigenetics in immune systems and provide promising references for future clinical treatment.
N6-methyladenosine (m6A) is the most abundant modification on mRNA and lncRNA. Numerous studies have shown that m6A modifications play important roles in RNA metabolisms, such as stability, translation, transportation, and localization. It has been recognized that m6A-related proteins, including methyltransferase (METTL3, METTL14, METTL16), demethylases (FTO, ALKBH5), ‘reader’ proteins (YTHDF1/2/3, YTHDC1/2, IGF2BP1/2/3), and other cooperated proteins that involved in m6A machinery, regulate normal tissue development and disease pathogenesis.
The immune system, which comprises innate immunity and adaptive immunity, protects our body from outside invaders. Innate immune cells include myeloid cells (macrophages, neutrophils, eosinophils, basophils, MDSCs, and dendritic cells), innate lymphoid cells (NK cells, ILC1, ILC2, ILC3, and LTi cells), ?d T cells, NKT cells, and mast cells. The adaptive immune system includes antigen-specific T cells, which are activated to proliferate through the action of APCs, and B cells which differentiate into plasma cells to produce antibodies.
RNA-mediated epigenetic regulation of cell functions and development is becoming more and more attractive. m6A modification is required for many processes in immune cells, including development, differentiation, activation, and polarization, thereby modulating the immune response. Our topic will mainly focus on the following aspects:
1. How m6A modifications regulate immune cell development, differentiation, or polarization. For example, the development of myeloid cells (macrophages, neutrophils, eosinophils, basophils, MDSCs, and dendritic cells), ?d T cells, NKT cells, and innate lymphoid cells (NK cells, ILC1, ILC2, ILC3, and LTi cells). T cell lineage (precursor T, memory T, etc.), and B cell lineage (progenitor B, precursor B, immature B, mature B, memory B).
2. Regulation of m6A machinery in immune cell-related diseases and neoplasms, for example, tumor or tumor microenvironment related/infiltrated immune cells, immune-related myeloid cells, tumor-infiltrated myeloid and lymphoid cells, immunosuppressive myeloid-derived suppressor cells, immunodeficiencies, autoimmune disease, hypersensitivity, idiopathic inflammation, B-cell leukemia (pre-B ALL), lymphoma (CLL, BCDCL, MCL, etc.), T-cell disease, T-cell leukemia, etc.
We are aiming to contribute to the basic studies of the full landscape of RNA epigenetics in immune systems and provide promising references for future clinical treatment.
