Table 3 RNA modifications and immune cells in infectious, inflammatory and autoimmune diseases
From: RNA modifications: importance in immune cell biology and related diseases
Type of immune disease | Involved disease | RNA modifications | Main functions | Ref. |
|---|---|---|---|---|
Infectious diseases | HIV-1 and VSV infection | m6A | Modified HIV-1 and VSV RNAs restrain the innate sensing efficacy of MDA5 or RIG-I and thereby impaired IFN-I-mediated innate antiviral immune responses in monocytes and macrophages. | |
VSV and HSV-1 infection | m6A | Inhibits viral replication and antiviral innate immunity via affecting various antiviral transcripts in in monocytes and macrophages. | ||
CMV-1 infection | m6A | Essential for the antiviral activity of NK cells by targeting Tardbp. | ||
COVID-19 infection | A-to-I editing | Edited endogenous Alu RNAs is decreased in normal human lung cells and in lung biopsies, possibly representing the responses of the hosts. | ||
Measles virus infection | A-to-I editing | Extensive duplex RNA structure edited by ADAR1 can lead to repressed innate immune responses and is profitable for viral replication. | ||
DNA and RNA virus infection | m6A, m5C, ac4C, Ψ, A-to-I editing | Affects RNA structure, RNA nuclear export, translation, stability, and replication. | ||
Inflammatory and autoimmune diseases | Hyperhomocysteinemia | m5C | NSUN2 upregulates IL-17A expression in an m5C-dependent manner in T lymphocytes. | |
Allergic asthma | m6A | Participates in the Th1/Th2 imbalance. | ||
IBD | m6A | Affects immune infiltration and therapeutic response. | ||
IBD | m6A | Mettl14 deficiency causes impaired induction of naïve T cells into iTreg cells by decreasing RORγt expression, contributing to spontaneous colitis. | ||
IBD | A-to-I editing | Impaired A-to-I editing due to Adar1 in CD4+ T cell leads to abnormal thymic T cell maturation and impaired negative selection, resulting in spontaneous colitis. | ||
Colon and lung Inflammation | m6A | IGF2BP2 switches M1 macrophages to M2 activation by stabilizing TSC1 and PPARγ in an m6A-dependent manner, leading to inflammatory diseases. | ||
Acute lung injury and respiratory distress syndrome | m6A | Ablation of METTL14 in myeloid cells exacerbates macrophage responses to acute bacterial infection. | ||
Liver fibrosis | m6A | Through essentially stimulating pyroptosis and inflammation of macrophages, the signaling cascade METTL3/MALAT1/PTBP1/USP8/TAK1 aggravates liver fibrosis. | ||
SLE | m5C | m5C level and NSUN2 expression are decreased in CD4+ T cells, and hypermethylated m5C is significantly involved in the immune- and inflammation-related pathways. | ||
SLE | ac4C | ac4C modification in mRNAs of SLE CD4+ T cells is highly enriched in CDS regions and involved in the immune and inflammatory signaling of SLE pathogenesis. | ||
SLE | A-to-I editing | Up-regulated ADAR1 in SLE T cells is a potential mechanism accounting for the mutations in the RI alpha subunit of type 1 protein kinase A. | ||
SLE | A-to-I editing | Involved in generating or elevating the autoantigen load. | ||
Autoimmune encephalomyelitis | m6A | Ablation of ALKBH5 resulted in increased m6A modification on IFNG and CXCL2 mRNA and impaired responses of CD4+ T cells, leading to repress autoimmunity. | ||
Systemic sclerosis | A-to-I editing | A-to-I editing mediated by ADAR1p150 in PBMCs are closely related to type I IFN responses. | ||
Allogeneic transplant | A-to-I editing | Edited RNA can suppress the host antigraft response and promote graft survival through the ADAR1-miR-21-Foxo1-IL-10 axis. |
