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Transcriptome analysis reveals LZ-8 triggers antiviral innate immunity in mouse T lymphocytes [RNASeq1]

ABSTRACT: 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.

ORGANISM(S): Mus musculus

PROVIDER: GSE199519 | GEO | 2025/03/28

REPOSITORIES: GEO

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Project description:Mesenchymal stem cells (MSCs) are known to induce the conversion of activated T-cells into regulatory T-cells in vitro. The marker CD69 is a target of canonical NF-κB signaling and is transiently expressed upon activation; however, stable CD69 expression defines cells with immunoregulatory properties. Given its enormous therapeutic potential, we explored the molecular mechanisms underlying the induction of regulatory cells by MSCs. Peripheral blood CD3+ T-cells were activated and cultured in the presence or absence of MSCs. CD4+ cell mRNA expression was then characterized by microarray analysis. The drug BAY11-7082 and a siRNA against RELB were used to explore the differential roles of canonical and non-canonical NF-κB signaling, respectively. Flow cytometry and real-time PCR were used for analyses. Genes with immunoregulatory functions, CD69 and non-canonical NF-κB subunits (RELB and NFKB2) were all expressed at higher levels in lymphocytes co-cultured with MSCs. The frequency of CD69+ cells among lymphocytes cultured alone progressively decreased after activation. In contrast, the frequency of CD69+ cells increased significantly following activation in lymphocytes co-cultured with MSCs. Inhibition of canonical NF-κB signaling by BAY immediately following activation blocked the induction of CD69; however, inhibition of canonical NF-κB signaling on the 3rd day further induced the expression of CD69. Furthermore, late expression of CD69 was inhibited by RELB siRNA. These results indicate that the canonical NF-κB pathway controls the early expression of CD69 after activation; however, in an immunoregulatory context, late and sustained CD69 expression is promoted by the non-canonical pathway and is inhibited by canonical NF-κB signaling. In order to study the molecular basis by which Multipotent Mesenchymal Stromal/Stem Cells (MSC) exert their immune regulatory function, immunomagnetically purified CD3+ T-cells from the peripheral blood of 3 individuals were activated and cultured in the presence or absence of MSCs. Following 5 days, CD4+ and CD8+ T-cells were further immunomagnetically selected and their gene expression profiles were obtained by microarrays and compared. Paired samples from 3 individuals were used for this analysis.

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Transcriptome analysis reveals LZ-8 triggers antiviral innate immunity in mouse T lymphocytes [RNASeq1]

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