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- Th0细胞通过表面黏附分子(T细胞表面的LFA-1、ICAM-1、CD2分别和APC的ICAM-1、LFA-1、LFA-3)和DC细胞发生短暂的可逆结合,有利于TCR特异性识别pMHCII(Ag-MHCII复合物)。 TCR:有αβ和γδ两种,αβT占95%由成簇的V、D、J基因节段以及恒定的C区基因间断排列而成基因重组酶参与TCR基因片段重排,遵循类似Ig的12/23法则TCRα和TCRβ都是
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- 当感染发生4天后,固有免疫进入适应性免疫应答诱导阶段。活化的巨噬细胞、DC加工抗原,并以Ag肽-MHC分子复合物的形式呈递到细胞表面,同时上调共刺激分子,为激活T细胞、启动适应性免疫应答创造条件。 活化的巨噬细胞留在原地巨噬细胞在PAMP分子和细胞因子如IFNγ刺激后,细胞表面MHC分子和共刺激分子水平上调,能够将Ag肽-MHC II分子复合物呈递给CD4+Th细胞。 抗原肽-MHC II分子的
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- 补体存在于血清、组织液和细胞表面,以非活性状态存在,本质是肝细胞、单核/巨噬细胞产生的糖蛋白酶原。当受到刺激时,补体各成份按顺序发生级联反应而激活。补体的活化有三条途径:旁路途径、MBL途径和经典途径。 补体活化的目的: 形成MAC(攻膜复合体),导致病原体细胞膜形成”渗漏斑”,破坏质子梯度形成杀伤 旁路途径 激活物提供保护性环境和接触表面:某些细菌细胞壁成分(LPS、葡聚糖)、酵母
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- 固有免疫应答分三个阶段:前四小时的瞬时阶段,前四天的早期阶段和之后的适应性免疫应答诱导阶段。瞬时阶段可终止绝大多数的病原体感染。 瞬时阶段病原体接触机体,首先遭到屏障结构的阻挡。 物理屏障:上皮细胞紧密连接、黏膜分泌黏液(被黏液包裹的微生物难以黏附表皮细胞)、纤毛摆动、尿液冲洗。 某些病原体会激活补体除经典途径外的途径,被裂解杀伤。产生的C5a/C3a可直接作用于肥大细胞,释放炎性介质
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- 人体免疫可分为固有免疫、适应性免疫和黏膜免疫。 固有免疫固有免疫是机体抵御病原体感染的第一道防线,无严格选择性,可对入侵的病原体迅速产生应答,并参与后续适应性免疫的启动、效应和调节。 适应性免疫适应性免疫分为B细胞介导的体液免疫和T细胞介导的细胞免疫。 黏膜免疫黏膜系统由黏膜上皮组织、黏膜相关淋巴组织、肠道共生菌群构成,参与免疫耐受的形成。
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- conda create -n clusterprofiler -c conda-forge r-base=4.1.2 -y conda activate clusterprofiler conda install -c conda-forge r-seurat=4.1.0 -y conda install -c conda-forge r-irkernel=1.3
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