The Promising Potential of Ezh1 Inhibition as a Therapeutic Strategy Against Dengue Infections
The investigation of enhancer of zeste homolog 1 (Ezh1) in the context of dengue infection immunity has been limited, necessitating further exploration to elucidate its precise role and underlying mechanisms during infections. To address this gap, we generated Ezh1 knockout mice and obtained bone ma...
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| Format: | Article |
| Language: | English |
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Wiley
2024-01-01
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| Series: | Journal of Immunology Research |
| Online Access: | http://dx.doi.org/10.1155/2024/5499761 |
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| author | Danping Liu Ningxin Tan Peidong Chi Junqi Huang |
| author_facet | Danping Liu Ningxin Tan Peidong Chi Junqi Huang |
| author_sort | Danping Liu |
| collection | DOAJ |
| description | The investigation of enhancer of zeste homolog 1 (Ezh1) in the context of dengue infection immunity has been limited, necessitating further exploration to elucidate its precise role and underlying mechanisms during infections. To address this gap, we generated Ezh1 knockout mice and obtained bone marrow and spleen samples from both Ezh1 knockout mice and wild-type (WT) counterparts. Leveraging RNA sequencing (RNA-seq) analysis, we identified the enrichment of genes associated with the interleukin-17 (IL-17) signaling pathway among the differentially expressed genes (DEGs) in the spleens of male Ezh1 knockout mice when compared to WT mice. Furthermore, our results revealed that Ezh1 knockout not only curtailed the viral load in dengue virus (DENV) infections but also suppressed the expression of pivotal cytokines, including interleukin-9 (IL-9) and IL-17. Additionally, utilizing high-parameter flow cytometry, we observed alterations in the immune cell phenotype within the spleens linked to Ezh1 gene knockout. Specifically, Ezh1 knockout inhibited the expressions of programmed cell death protein 1 (PD-1), lymphocyte-activation gene 3 (LAG-3), and cluster of differentiation 86 (CD86). Additionally, we noted a reduction in cluster of differentiation 62L (CD62L) expression in neutrophils following DENV infection. Our comprehensive findings collectively underscore the significant role of Ezh1 in DENV infection, suggesting that targeting Ezh1 could offer a promising antiviral strategy. |
| format | Article |
| id | doaj-art-4e8b2951db7c4b66b534e0bae9e700d0 |
| institution | OA Journals |
| issn | 2314-7156 |
| language | English |
| publishDate | 2024-01-01 |
| publisher | Wiley |
| record_format | Article |
| series | Journal of Immunology Research |
| spelling | doaj-art-4e8b2951db7c4b66b534e0bae9e700d02025-08-20T01:54:15ZengWileyJournal of Immunology Research2314-71562024-01-01202410.1155/2024/5499761The Promising Potential of Ezh1 Inhibition as a Therapeutic Strategy Against Dengue InfectionsDanping Liu0Ningxin Tan1Peidong Chi2Junqi Huang3Organ Transplant CenterOrgan Transplant CenterState Key Laboratory of Oncology in South ChinaOrgan Transplant CenterThe investigation of enhancer of zeste homolog 1 (Ezh1) in the context of dengue infection immunity has been limited, necessitating further exploration to elucidate its precise role and underlying mechanisms during infections. To address this gap, we generated Ezh1 knockout mice and obtained bone marrow and spleen samples from both Ezh1 knockout mice and wild-type (WT) counterparts. Leveraging RNA sequencing (RNA-seq) analysis, we identified the enrichment of genes associated with the interleukin-17 (IL-17) signaling pathway among the differentially expressed genes (DEGs) in the spleens of male Ezh1 knockout mice when compared to WT mice. Furthermore, our results revealed that Ezh1 knockout not only curtailed the viral load in dengue virus (DENV) infections but also suppressed the expression of pivotal cytokines, including interleukin-9 (IL-9) and IL-17. Additionally, utilizing high-parameter flow cytometry, we observed alterations in the immune cell phenotype within the spleens linked to Ezh1 gene knockout. Specifically, Ezh1 knockout inhibited the expressions of programmed cell death protein 1 (PD-1), lymphocyte-activation gene 3 (LAG-3), and cluster of differentiation 86 (CD86). Additionally, we noted a reduction in cluster of differentiation 62L (CD62L) expression in neutrophils following DENV infection. Our comprehensive findings collectively underscore the significant role of Ezh1 in DENV infection, suggesting that targeting Ezh1 could offer a promising antiviral strategy.http://dx.doi.org/10.1155/2024/5499761 |
| spellingShingle | Danping Liu Ningxin Tan Peidong Chi Junqi Huang The Promising Potential of Ezh1 Inhibition as a Therapeutic Strategy Against Dengue Infections Journal of Immunology Research |
| title | The Promising Potential of Ezh1 Inhibition as a Therapeutic Strategy Against Dengue Infections |
| title_full | The Promising Potential of Ezh1 Inhibition as a Therapeutic Strategy Against Dengue Infections |
| title_fullStr | The Promising Potential of Ezh1 Inhibition as a Therapeutic Strategy Against Dengue Infections |
| title_full_unstemmed | The Promising Potential of Ezh1 Inhibition as a Therapeutic Strategy Against Dengue Infections |
| title_short | The Promising Potential of Ezh1 Inhibition as a Therapeutic Strategy Against Dengue Infections |
| title_sort | promising potential of ezh1 inhibition as a therapeutic strategy against dengue infections |
| url | http://dx.doi.org/10.1155/2024/5499761 |
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