scholarly journals Long Noncoding RNA AW112010 Promotes the Differentiation of Inflammatory T Cells by Suppressing IL-10 Expression through Histone Demethylation

2020 ◽  
Vol 205 (4) ◽  
pp. 987-993 ◽  
Author(s):  
Xiaoming Yang ◽  
Marpe Bam ◽  
William Becker ◽  
Prakash S. Nagarkatti ◽  
Mitzi Nagarkatti
Keyword(s):  
T Cells ◽  
Long Noncoding Rna ◽  
Noncoding Rna ◽  
Histone Demethylation

LncRNA-ENST00000421645 promotes T cells to secrete IFN-γ by sponging PCM-1 in neurosyphilis

Epigenomics ◽  
2021 ◽  
Author(s):  
Wen-Na Liu ◽  
Kai-Xuan Wu ◽  
Xiao-Tong Wang ◽  
Li-Rong Lin ◽  
Man-Li Tong ◽  
...  
Keyword(s):  
Flow Cytometry ◽  
T Cells ◽  
Peripheral Blood ◽  
Long Noncoding Rna ◽  
Noncoding Rna ◽  
Chip Assay ◽  
Rna Immunoprecipitation ◽  
Ifn Γ ◽  
Significant Expression

Aim: Neurosyphilis patients exhibited significant expression of long noncoding RNA (lncRNA) in peripheral blood T lymphocytes. In this study, we further clarified the role of lncRNA- ENST00000421645 in the pathogenic mechanism of neurosyphilis. Methods: lncRNA- ENST00000421645 was transfected into Jurkat-E6-1 cells, namely lentivirus (Lv)-1645 cells. RNA pull-down assay, flow cytometry, RT-qPCR, ELISA (Neobioscience Technology Co Ltd, Shenzhen, China) and RNA immunoprecipitation chip assay were used to analyze the function of lncRNA- ENST00000421645. Results: The expression of IFN-γ in Lv-1645 cells was significantly increased compared to that in Jurkat-E6-1 cells stimulated by phorbol-12-myristate-13-acetate (PMA). Then, it was suggested that lncRNA- ENST00000421645 interacts with PCM1 protein. Silencing PCM1 significantly increased the level of IFN-γ in Lv-1645 cells stimulated by PMA. Conclusion: This study revealed that lncRNA- ENST00000421645 mediates the production of IFN-γ by sponging PCM1 protein after PMA stimulation.

scholarly journals Long noncoding RNA derived from CD244 signaling epigenetically controls CD8+ T-cell immune responses in tuberculosis infection

2015 ◽  
Vol 112 (29) ◽  
pp. E3883-E3892 ◽  
Author(s):  
Yang Wang ◽  
Huiling Zhong ◽  
Xiaodan Xie ◽  
Crystal Y. Chen ◽  
Dan Huang ◽  
...  
Keyword(s):  
T Cells ◽  
T Cell ◽  
Immune Responses ◽  
Long Noncoding Rna ◽  
Noncoding Rna ◽  
Molecular Mechanisms ◽  
Cell Subpopulation ◽  
Tnf Α ◽  
T Cell Immune Responses ◽  
Ifn Γ

Molecular mechanisms for T-cell immune responses modulated by T cell-inhibitory molecules during tuberculosis (TB) infection remain unclear. Here, we show that active human TB infection up-regulates CD244 and CD244 signaling-associated molecules in CD8+ T cells and that blockade of CD244 signaling enhances production of IFN-γ and TNF-α. CD244 expression/signaling in TB correlates with high levels of a long noncoding RNA (lncRNA)-BC050410 [named as lncRNA-AS-GSTT1(1-72) or lncRNA-CD244] in the CD244+CD8+ T-cell subpopulation. CD244 signaling drives lncRNA-CD244 expression via sustaining a permissive chromatin state in the lncRNA-CD244 locus. By recruiting polycomb protein enhancer of zeste homolog 2 (EZH2) to infg/tnfa promoters, lncRNA-CD244 mediates H3K27 trimethylation at infg/tnfa loci toward repressive chromatin states and inhibits IFN-γ/TNF-α expression in CD8+ T cells. Such inhibition can be reversed by knock down of lncRNA-CD244. Interestingly, adoptive transfer of lncRNA-CD244–depressed CD8+ T cells to Mycobacterium tuberculosis (MTB)-infected mice reduced MTB infection and TB pathology compared with lncRNA-CD244–expressed controls. Thus, this work uncovers previously unidentified mechanisms in which T cell-inhibitory signaling and lncRNAs regulate T-cell responses and host defense against TB infection.

scholarly journals Long Noncoding RNA GM16343 Promotes IL-36β to Regulate Tumor Microenvironment by CD8+T cells

2019 ◽  
Vol 18 ◽  
pp. 153303381988363 ◽  
Author(s):  
Deli Mao ◽  
Chenrui Hu ◽  
Jianglei Zhang ◽  
Chao Feng ◽  
Zhe Zhang ◽  
...  
Keyword(s):  
T Cells ◽  
Survival Time ◽  
Long Noncoding Rna ◽  
Noncoding Rna ◽  
Interferon Γ ◽  
Control Group ◽  
Tumor Diameter ◽  
Chain Reaction ◽  
Polymerase Chain ◽  
The Difference

Objective: To investigate the effect of long noncoding RNA GM16343 on interleukin 36β promotion of CD8+T cells in tumor microenvironment regulation. Methods: The differentially expressed long noncoding RNA in interleukin 36β-stimulated mouse CD8+T cells was screened by gene chip technology, and the significant differentially expressed long noncoding RNAs were verified by real-time polymerase chain reaction. The lentiviral vector that overexpresses or knockdown GM16343 was constructed, transfected into CD8+T cells, and stimulated with interleukin 36β, and the amount of interferon γ secreted was detected by enzyme-linked immunosorbent assay. A mouse subcutaneous xenograft model that stably express interleukin 36β was established, and the tumor size and mouse survival time were observed by stimulation with CD8+T cells overexpression or knockdown of GM16343. Results: A total of 12 long noncoding RNAs with significant differences were screened by gene chip analysis. Real-time polymerase chain reaction showed that the difference in GM16343 was larger, and the difference between the groups was observed to be the most significant. Compared to control group, CD8+T cells overexpressing GM16343 increased the secretion of interferon γ, and the tumor diameter of the mice after stimulation showed significant reduction, and the survival time showed significant prolongation. Compared to control group, the CD8+T cells after GM16343 were knocked down. The interferon γ secretion was decreased, and no significant change in tumor diameter and survival time was observed. Conclusion: Interleukin 36β may enhance antitumor immune response of CD8+T cells by regulating GM16343.

scholarly journals Viral apoptosis evasion via the MAPK pathway by use of a host long noncoding RNA

2017 ◽  
Author(s):  
Samantha Barichievy ◽  
Jerolen Naidoo ◽  
Mikaël Boullé ◽  
Janine Scholefield ◽  
Suraj P. Parihar ◽  
...  
Keyword(s):  
T Cells ◽  
Long Noncoding Rna ◽  
Cd4 T Cells ◽  
Noncoding Rna ◽  
Cellular Response ◽  
Dna Lesions ◽  
Host Cells ◽  
Dependent Manner ◽  
Hnrnp K ◽  
Hiv 1

SUMMARYAn emerging realisation of infectious disease is the high incidence of genetic instability resulting from pathogen-induced DNA lesions, often leading to classical hallmarks of cancer such as evasion of apoptosis. The Human Immunodeficiency Virus type 1 (HIV-1) induces apoptosis in CD4+ T cells but is largely non-cytopathic in macrophages, thereby leading to long-term dissemination of the pathogen specifically by these host cells. Apoptosis is triggered by double-strand breaks (DSBs), such as those induced by integrating retroviruses, and is coordinated by the p53-regulated long noncoding RNA lincRNA-p21, in a complex with its protein binding partners HuR and hnRNP-K. Here, we monitor the cellular response to infection to determine how HIV-1 induces DSBs in macrophages yet evades apoptosis in these cells. We show that the virus does so by securing the pro-survival MAP2K1/ERK2 cascade early upon entry, in a gp120-dependent manner, to orchestrate a complex dysregulation of lincRNA-p21. By sequestering HuR in the nucleus, HIV-1 enables lincRNA-p21 degradation. Simultaneously, the virus permits transcription of pro-survival genes by sequestering hnRNP-K in the cytoplasm via the MAP2K1/ERK2 pathway. Notably, this pro-survival cascade is unavailable for similar viral manipulation in CD4+ T cells. The introduction of MAP2K1, ERK2 or HDM2 inhibitors in HIV-infected macrophages results in apoptosis providing strong evidence that the viral-mediated apoptotic block can be released, specifically by restoring the nuclear interaction of lincRNA-p21 and hnRNP-K. These results reveal pathogenic control of apoptosis and DNA damage via a host long noncoding RNA, and present MAP2K1/ERK2 inhibitors as a novel therapeutic intervention strategy for HIV-1 infection in macrophages.

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