Transcriptome analysis reveals LZ-8 triggers antiviral innate immunity in mouse T lymphocytes [RNASeq1]
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ABSTRACT:
PROVIDER: PRJNA820611 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR18500457.fastq.gz | Fastqsanger.gz | |||
| SRR18500458.fastq.gz | Fastqsanger.gz | |||
| SRR18500459.fastq.gz | Fastqsanger.gz | |||
| SRR18500460.fastq.gz | Fastqsanger.gz | |||
| SRR18500461.fastq.gz | Fastqsanger.gz |
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Project description:Ganoderma lucidum is a traditional medicinal herb that has commonly been used for treating virus infections. Protein LZ-8 comes from Ganoderma lucidum and has immunomodulatory and antiviral activities. However, the potential molecular antiviral mechanism of LZ-8 is still unclear. In this study transcriptome analysis was used to gain a deeper insight into the antiviral effects of LZ-8 on T lymphocytes. Deseq analysis showed that 2724 genes were upregulated and 3314 genes were downregulated after LZ-8 treatment for 5 hours. GO enrichment analysis showed that the upregulated genes were significantly enriched in biological processes including defense response to virus, ribosome biosynthesis, RNA processing, etc. The downregulated genes were significantly enriched in biological processes including cell cycle, signal transduction, etc. Pathway enrichment analysis indicated that NF- κB signaling pathway was closely related to LZ-8. RT-qPCR confirmed that inhibition of the NF-κB signaling pathway reversed the elevated transcriptional level of antiviral genes including Ifit1, Isg15, Mx1, Ifit3, and Ifih1 in T lymphocytes triggered by LZ-8. In a word, our study demonstrated that LZ-8 triggered the antiviral innate immunity of T lymphocytes through the NF-κB signaling pathway.
2025-03-28 | GSE199519 | GEO
Project description:LZ-8 is an immunomodulatory protein derived from the large edible fungus Ganoderma lucidum. LZ-8 has therapeutic effects on several disorders of the immune system. T lymphocytes are considered to be one of the target cells of LZ-8. In order to comprehensively and systematically study the immunomodulatory effect of LZ-8 on T lymphocytes at the transcriptome level, we used RNA-seq technology to sequence the transcriptome of mouse T lymphocytes treated with LZ-8 for 10 hours and 0 hour. Differential gene analysis showed that 1275 genes were up-regulated and 2273 genes were down regulated after LZ-8 treatment for 10h. The pathway enrichment analysis showed that differential genes were enriched in terms of "Th1 and Th2 cell differentiation", "Th17 cell differentiation" and "IL-17 signaling pathway". RT-qPCR experiment confirmed that LZ-8 could upregulate the transcription level of Il4, Il13, Il17f and Csf2 in T lymphocytes, and the inhibitor Bay 11-7082 which inhibited NF κ B signaling pathway can reverse the transcriptional upregulation of Il2, Il17a and Irf4 by LZ-8. In conclusion, transcriptome sequencing data combined with RT-qPCR confirmed the promoting effect of LZ-8 on Th17 differentiation.
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Project description:Innate immunity serves as the primary defense against viral and microbial infections in humans. Among its components, retinoic acid-inducible gene I (RIG-I)-like receptors (RLRs) are well-characterized intracellular pattern-recognition proteins that trigger innate immune responses upon viral infection. However, the precise influence of cellular metabolites, especially fatty acids, on the regulation of RLR-mediated antiviral innate immunity remains largely elusive. Here, through screening a metabolite library, palmitic acid (PA) has been identified as a crucial metabolite responsible for modulating antiviral infections. Mechanistically, PA induces the palmitoylation of MAVS, leading to MAVS aggregation and subsequent activation, thereby enhancing the innate immune response against viral infections. Functionally, the enzyme palmitoyl-transferase ZDHHC24 plays a key role in catalyzing the palmitoylation of MAVS at both C46 and C79 residues, thereby facilitating the transduction of RLR-mediated TBK1-IRF3-IFN signaling pathway, particularly under conditions of PA stimulation or high-fat diet feeding. Conversely, the absence of ZDHHC24 significantly attenuates virus-induced innate immune responses in both cells and mice. Moreover, APT2 counteracts with ZDHHC24 to de-palmitoylate MAVS, thus inhibiting the antiviral response. Consequently, inhibition of APT2 using compounds like ML349 effectively reverses MAVS palmitoylation and activation in response to antiviral infections. These findings underscore the critical role of PA and ZDHHC24 in regulating antiviral innate immunity through MAVS palmitoylation, and suggest potential therapeutic strategies for combating viral infections, such as enhancing PA intake or specifically targeting APT2.
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Project description:LZ-8 is a dimeric protein isolated from Ganoderma lucidum. It has immunomodulatory activity on T cells. In order to fully analyze the immunomodulatory effect of LZ-8 on CD4 + T cells and CD8 + T cells, we first sequenced the transcriptome of mouse T lymphocytes treated with LZ-8 for 15 hours, then compared the differential genes regulated by LZ-8 with those activated in CD4 + T cells and CD8 + T cells in GSE126116 data, and finally obtained the core biological process and signal pathway induced by LZ-8 to regulating the activation state of CD4 + T cells and CD8 + T cells.
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Project description:TBK1 plays a pivotal role in innate antiviral immunity, serving as a critical mediator downstream of various pattern recognition receptors (PRRs). TBK1 activity is tightly regulated by post-translational modifications (PTMs) including ubiquitination to maintain innate immune homeostasis. Here, we identify the Deltex E3 ubiquitin ligase 2 (DTX2) as a positive regulator of innate antiviral signaling in response to RNA viruses. We find that DTX2 overexpression enhances antiviral signaling, whereas loss of DTX2 evidently reduces antiviral responses. Mechanistically, we demonstrated that DTX2 directly interacts with TBK1 and promotes TBK1 K63-linked polyubiquitination to regulate antiviral signaling. Collectively, our study reveals that DTX2 plays a novel positive regulatory role in antiviral signaling by modulating the K63-linked ubiquitination of TBK1 to maintain the balance of innate antiviral immune responses.
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Project description:Dendritic cells (DC) serve a key function in host defense, linking innate detection of microbes to the activation of pathogen-specific adaptive immune responses. Whether there is cell-intrinsic recognition of HIV-1 by host innate pattern-recognition receptors and subsequent coupling to antiviral T cell responses is not yet known. DC are largely resistant to infection with HIV-1, but facilitate infection of co-cultured T-helper cells through a process of trans-enhancement. We show here that, when DC resistance to infection is circumvented, HIV-1 induces DC maturation, an antiviral type I interferon response and activation of T cells. This innate response is dependent on the interaction of newly-synthesized HIV-1 capsid (CA) with cellular cyclophilin A (CypA) and the subsequent activation of the transcription factor IRF3. Because the peptidyl-prolyl isomerase CypA also interacts with CA to promote HIV-1 infectivity, our results suggest that CA conformation has evolved under opposing selective pressures for infectivity versus furtiveness. Thus, a cell intrinsic sensor for HIV-1 exists in DC and mediates an antiviral immune response, but it is not typically engaged due to absence of DC infection. The virulence of HIV-1 may be related to evasion of this response, whose manipulation may be necessary to generate an effective HIV-1 vaccine. We analyzed the gene expression profiles of uninfected human monocyte-derived dendritic cells (MDDCs) and MDDCs infected with an envelope-defective GFP-encoding VSV-G-pseudotyped HIV-1 vector (HIVGFP(G)) and with VSV-G pseudotyped virus-like particles derived from SIVmac to deliver Vpx (SIVVLP(G)), alone or in combination. Cells were infected at day 4 of differentiation and cells were harvested 48 hours later. RNA was extracted with TRIzol. RNA was labeled and hybridized to Human Genome U133A 2.0 arrays arrays following the Affymetrix protocols. Data were analyzed in R and Bioconductor.
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