免疫调节达人之细胞因子— IL-4 - 知乎 - 知乎专栏
IL-4 促进 B 细胞 MHCⅡ类抗原、FcεRⅡ/CD23 和 CD40 的表达，并增强 B 细胞提呈抗原能力，使免疫系统对小量抗原刺激发生免疫应答。 增加 FcεRⅡ/CD23 (IgE Fc 段低亲和力受体) 的 …
CD4+/IL‑4+ lymphocytes of the lamina propria and substance P …
Moreover, it was found that acute stress caused a shift towards a predominantly anti‑inflammatory immune response (T helper 2 cells), as shown by the increase in the percentage of CD4 + …
白细胞介素 4（IL-4） - 丁香通研选
2017年8月31日 · IL-4 促进 B 细胞 MHCⅡ类抗原、FcεRⅡ/CD23 和 CD40 的表达，并增强 B 细胞提呈抗原能力，使免疫系统对小量抗原刺激发生免疫应答。 增加 FcεRⅡ/CD23 (IgE Fc 段低 …
The differential expression of IL-4 and IL-13 and its impact on …
This review summarizes the literature surrounding the function and expression of IL-4 and IL-13 in CD4+ T cells and innate immune cells. It highlights recent in vivo findings regarding the …
Frontiers | IL-4 Is a Key Requirement for IL-4- and IL-4/IL-13 ...
We sought to better define IL-4’s role in CD4 Th2 responses by using transgenic mice that express a dual IL-4 AmCyan/IL-13 DsRed (IL-4AC/IL-13DR) fluorescent reporter on an IL-4 …
Recent advances in understanding the role of IL-4 signaling
IL-4 induces elevated cell surface expression of CD23 (the low-affinity IgE receptor) on B cells and of class II major histocompatibility complex (MHC) molecules. In addition, IL-4 acts as a T …
IL-4 drives exhaustion of CD8 + CART cells - Nature
2024年9月12日 · Further, IL-4-treated CD8 + CART cells develop signs of exhaustion independently of the presence of CD4 + CART cells. Conversely, IL-4 pathway editing or the …
免疫调节因子-IL-4 - 知乎 - 知乎专栏
IL-4促进B细胞MHCⅡ类抗原、 FcεRⅡ/CD23 和 CD40 的表达，并增强B细胞提呈抗原能力，使免疫系统对小量抗原刺激发生免疫应答。 增加FcεRⅡ/CD23 (IgE Fc 段低亲和力受体) 的表达， …
STAT3 determines IL-4 signalling outcomes in naïve T cells
2021年5月18日 · Mounting evidence indicates that cells can dynamically alter their IL-4/IL-13 receptor signature to modulate downstream immune outcomes upon pathogen encounter. …
The type 2 cytokine Fc–IL-4 revitalizes exhausted CD8 - Nature
2024年9月25日 · Here we show that an interleukin-4 fusion protein (Fc–IL-4), a typical type 2 cytokine, directly acts on CD8 + T cells and enriches functional terminally exhausted CD8 + T …
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