Nature Sub-Journal: Cao Xuetao's team has reissued a top-level paper, making new advances in congenital immunity, revealing a new type of non-coding RNA regulatory network.

Innate immune response can protect host from pathogen infection and exert evolutionary pressure on pathogen to weaken these reactions and ensure their survival and replication.these changing pressures lead to complex mechanisms of innate immune homeostasis in cross host pathogen interactions, but they have not been fully understood.in particular, a better understanding of the regulators that control host pathogen interactions and facilitate the clearance or escape of invasive pathogens can identify therapeutic targets for infectious diseases and chronic inflammation.non coding RNA (ncRNA) regulates various innate and adaptive immune processes.MicroRNA (miRNA) is the most in-depth ncRNA studied. It usually acts as a transcriptional regulator in gene expression in immune response, and long chain non encoding RNA (lncRNA) has become the other key regulator of gene expression in various physiology.lncrna regulates signal transduction pathways in immune response and inflammation through a variety of mechanisms, including acting as a guide, scaffold or bait for regulatory proteins.interferon - γ (IFN - γ) is essential for the innate immune response of intracellular bacteria.the role of non coding RNA and RNA binding protein (RBP) in the regulation of IFN - γ activated signaling pathway in macrophages is not very clear.on November 18, 2019, Cao Xuetao's team published a research paper entitled "induced degradation of lncrna sros1 promotes IFN - γ - mediated activation of innate immune responses by stabilizing STAT1 mRNA in Nature Immunology.this study found that miR-1 promoted IFN - γ - mediated Listeria clearance in macrophages by degrading lncrna sros1 and indirectly stabilizing STAT1 mRNA.inducible degradation or genetic deletion of sros1 results in IFN - γ dependent activation of enhanced innate immune response.in terms of mechanism, sros1 blocks the binding of STAT1 mRNA with RBP caprin1, thus stabilizing STAT1 mRNA and promoting IFN - γ - STAT1 mediated innate immunity.these findings reveal a complex RNA-RNA regulatory network involved in innate cytokine induced responses in host pathogen interactions.nuclear lncrnas regulate the transcription of immune response genes through subnuclear structure of scaffold and guidance of nucleosome localization.lncrna – acod1 directly binds to its enzyme chaperone glutamic acid oxaloacetate transaminase 2 to enhance the catalytic activity of the enzyme and promote virus infection.despite these observations, the range and setting of lncrnas that regulate host pathogen interactions are unclear.in addition, the multiple mechanisms by which lncrnas are used to regulate innate immune responses to bacterial infections make it difficult to predict whether and how lncrnas are involved. Listeria monocytogenes is an intracellular pathogenic Gram-positive bacterium, which is an ideal model for studying host pathogen interaction and intracellular infection. Listeria monocytogenes can be transformed into pathogens after ingested by susceptible eukaryotic hosts to survive in harsh environments. the fate of infection depends on the balance between macrophage activation and pathogen resistance to host cell bactericidal activity. interferon type II (IFN - γ) has effective anti microbial activity through signal converter Jak and transcription activator stat. the transcription factor can activate macrophages against intracellular microorganisms. in order to solve how the number of STAT1 can balance in the immune response, this study screened miRNAs that interact between Listeria monocytogenes and macrophages. researchers found that miR-1 promoted IFN - γ - mediated innate responses in macrophages to Listeria monocytogenes infection. miR-1 increased STAT1 mRNA expression and enhanced IFN - γ signal transduction in macrophages after transcription. in an unbiased miRNA in vivo precipitation (mirip) method, lncrna sros1 (an inhibitory non coding RNA of STAT1) was found to be targeted by miR-1. miR-1 mediated sros1 degradation can stabilize STAT1 mRNA and promote IFN - γ - STAT1 mediated innate response. in conclusion, these findings reveal a complex RNA-RNA regulatory network involved in innate cytokine induced responses in host pathogen interactions. < br / < br / < br / < br / < br / < br / < br / < br / < br / < br / < br / < br / < br / < br / < br / < br / < br / < br / < br / < br / < br / < br / < br / < br / < br / < br / < br / < br / < br / < br / < br / < br / < br / < br / < br / < br / < br / < br / < br / < br / < br / < br / < br / < br / < br / < br / < br / < br / < br / < br / < br / < br / link: This article is from: inature: inature, click to view the related articles: CRISPR | ngago | ngago: cna cancer treatment hot tomato prion cell membrane