Downregulation of IRF7-mediated type-I interferon response by
2024年12月19日 · We found that immunization with LmCen–/– induces a transient increase in type I IFN response along with its regulatory factor IRF7 that is downregulated 7–21 days post …
Interferon regulatory factor 7 in inflammation, cancer and infection
Interferon regulatory factor 7 (IRF7), a member of the interferon regulatory factors (IRFs) family, is located downstream of the pattern recognition receptors (PRRs)-mediated signaling pathway …
IFN-γ–producing TH1 cells and dysfunctional regulatory T cells ...
2024年12月18日 · An IPA upstream regulator analysis of FOXP3 + T reg cells showed a robust enrichment of molecules involved in type I, II, and III IFN signaling, including IFNA2, IFNG, …
Interferon regulatory factor-7 modulates experimental …
Interferon regulatory factor 7 (IRF7) is critical for the induction and positive feedback regulation of type I IFN. To establish whether and how endogenous type I IFN signaling contributes to …
PNAS：南方医科大学毕恩广团队研究表明IFN-γ诱导的I型干扰素应答网络通过IRF7增强th17来源的Th1 …
2024年11月14日，南方医科大学毕恩广，徐啊白和Yu Hu共同通讯在PNAS 在线发表题为 “Augmenting antitumor efficacy of Th17-derived Th1 cells through IFN-γ-induced type I …
毕恩广团队在T细胞亚群发现及弥漫大B淋巴瘤治疗机制方面取得新 …
2024年11月19日 · 在实体肿瘤治疗中，当前T细胞疗法的疗效受限于T细胞耗竭和肿瘤浸润不足。研究团队发现了一种由Th17细胞衍生的Th1细胞亚群（Th 17 1），这种细胞在抗肿瘤能力上 …
Augmenting antitumor efficacy of Th17-derived Th1 cells through …
Furthermore, we show that IFN-γ up-regulated IRF7 to promote the type I interferon response network and ECM1 expression but decreased the exhaustion status in Th 17 1 cells. Taken …
PNAS：南方医科大学毕恩广团队研究表明IFN-γ诱导的I型干扰素应答网络通过IRF7增强th17来源的Th1 …
南方医科大研究发现肿瘤内 Th171 细胞，具强抗肿瘤力且耗竭少，源于 Th17 后转分化，IFN -γ 经 IRF7 促其低耗竭与高 ECM1 表达，为抗癌策略添思路。 在癌症免疫治疗中，CD4+ T细胞的重 …
PNAS丨南方医科大学毕恩广团队研究表明IFN-γ诱导的I型干扰素应答网络通过IRF7增强th17来源的Th1 …
2024年11月21日 · 研究发现，Th171细胞通过IFN-γ诱导的I型干扰素应答网络，特别是通过IRF7的调节，增强了其抗肿瘤功效。 Th171细胞在体外培养中表现出与肿瘤浸润性Th171细胞高度相 …
IRFs: master regulators of signalling by Toll-like receptors and ...
2006年9月1日 · IRF7 is essential for the robust type I IFN gene induction that is elicited by ligation of TLR7 or TLR9, whereas IRF5 is required for the induction of pro-inflammatory cytokine …