Treg细胞在Chatfl/fl; Cd4-cre小鼠中阻断HCC免疫监视,T细胞ChAT缺失会加剧HCC中T细胞功能障碍。 04TCR诱导的Ca2+-NFAT信号传导的胆碱能调节 为了确定胆碱能活性是否影响T细胞中的Ca2+信号传导,作者开展了一系列信号转导通路检测。发现与Chatfl/fl相比,TCR参与引起的Ca2+内流在Chatfl/fl;Cd4-cre T细胞中明显增强。...
We generateddistal Lck (dLck)-cre mice, with deletion of autophagy only at a mature stage. In this model, autophagy deficiency impacts CD8T cell survival but has no influence on CD4T cell number and short-term activation. Moreover, autophagy in T cells is dispensable during early humoral ...
使用OVA来模拟肿瘤抗原表明其能驱动胆碱能CD4+T细胞扩增。 通过将条件性敲除Chatfl小鼠与Cd4-cre小鼠杂交,特异性地删除了T细胞中的ChAT,从而获得了Chatfl/fl;Cd4-cre后代。在诱导HCC时,发现Chatfl/fl; Cd4-cre小鼠比Chatfl/fl小鼠更快产生肿瘤。T细胞中Chat的敲除阻碍了适应性和先天性抗肿瘤免疫反应,抑制了HCC的...
Fig3. Expression characterization of hCD4 in hCD4 KI mice. 相关品系 hCD40 品系名:C57BL/6Smoc-Cd40em1(hCD40) Smoc 品系状态:活体 | 目录号:NM-HU-00076 Apoe-KO/hSIRPA/hCD47 品系名:C57BL/6Smoc-Apoeem5Sirpatm2(hSIRPA)Cd47em1(hCD47)Smoc 品系状态:活体 | 目录号:NM-XA-241005 Cd44-...
通过同源重组,将小鼠Cd4基因进行人源化修饰。 应用领域:免疫治疗;肿瘤研究;药物筛选 *使用本品系发表的文献需注明: hCD4 mice (Cat. NO. NM-HU-00115) were purchased from Shanghai Model Organisms Center, Inc.. 验证数据 Fig 1. Flow cytometric analysis of the T cell subtype proportions in peripheral...
在诱导HCC时,发现Chatfl/fl; Cd4-cre小鼠比Chatfl/fl小鼠更快产生肿瘤。T细胞中Chat的敲除阻碍了适应性和先天性抗肿瘤免疫反应,抑制了HCC的免疫监视。Treg细胞在Chatfl/fl; Cd4-cre小鼠中阻断HCC免疫监视,T细胞ChAT缺失会加剧HCC中T细胞功能障碍。 04.TCR诱导的Ca2+-NFAT信号传导的胆碱能调节...
(dLck)-cre mice, with deletion of autophagy only at a mature stage. In this model, autophagy deficiency impacts CD8+T cell survival but has no influence on CD4+T cell number and short-term activation. Moreover, autophagy in T cells is dispensable during early humoral response but critical ...
In addition, in this model, BCC are not caused by malfunctioning of Ptch-deficient T cells, as BCC did not develop when bone marrow (BM) of Ptch(flox/flox)CD4Cre(+/-) mice was transplanted into Ptch wild-type mice. Instead, lineage-tracing experiments and flow cytometric analyses suggest...
To study molecular mechanisms of peripheral CD4-T-cell differentiation in-vivo and in-vitro we generated transgenic mice expressing a tamoxifen inducible Cre recombinase (CreERT2) under the control of the CD4 gene promoter. We show here that in CD4CreERT2 mice Cre is inducibly and selectively act...
Our laboratory analyzed mice with a combined T cell-specific deletion (using Cd4-Cre) of Hdac1 and Hdac2 (HDAC1-2cDKO). This study revealed an HDAC1-2-controlled plasticity of CD4+ T cells towards the CD8+ T cell lineage [131]. In HDAC1-2cDKO mice, a fraction of peripheral MHC class...