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  113. 实用免疫学(十一)白细胞分化番外篇一:胚系基因重排
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  118. 胚系基因的结构TCR胚系基因 免疫球蛋白胚系基因 胚系基因重排TCR基因重排 免疫球蛋白基因重排 胚系基因重组与连接RSS(重组信号序列) 一些位于Ig 和 TCR可变区基因片段外显子旁侧、与可变区基因片段重排有关的 DNA序列 RSS包括一个高度保守的、具有回文结构的7核苷酸序列(heptamer,CACAGTG),总是紧邻V、D和J基因的外显子 两者之间、非保守的 12或 23碱基对(bp)间
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  125. 2022-03-23
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  143. 实用免疫学(十)免疫细胞分化关系树
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  148. 血细胞由造血器官产生,人胚胎时期的卵黄囊、肝、脾、胸腺和骨髓等器官均具有造血功能,出生后,红骨髓是主要的造血器官。 血岛是人类胚胎最早形成血细胞的场所:人胚第三周,卵黄囊壁等处的胚外中胚层细胞团聚而成血岛,开始出现原始的造血干细胞,但仅能向红细胞系分化造血,称为原始造血或胚胎造血。 人胚第6周初,造血干细胞随血流迁移至肝,肝开始造血。 第9~20周,胎肝是体内主要的造血场所。脾造血也于胚胎第
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  155. 2022-03-07
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  173. 实用免疫学(九)适应性免疫番外篇二:抗原呈递
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  178. 外源性抗原肽通过MHCII呈递,内源性抗原通过MHCI呈递,此外还有交叉呈递和脂类抗原的提呈途径 交叉提呈途径 APC将外源性抗原通过MHCI类分子途径提呈给CD8+T细胞 从晚期内体/吞噬溶酶体溢出进入胞质/直接进入胞质 晚期内体/吞噬溶酶体中形成的抗原肽胞吐出胞、和膜表面的空载MHCI类分子结合而被提呈 细胞表面MHCI类分子被重新内吞进入内体/新合成的MHCI类分子进入内体,直接和外源
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  184. <time datetime="2022-03-07 11:39" pubdate>
  185. 2022-03-07
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  203. 实用免疫学(六)适应性免疫:细胞免疫二 CTL细胞
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  208. DC细胞提呈外源性抗原激活Th细胞,对于内源性抗原和进入细胞内的抗原,则通过所有有核细胞的MHCI类分子进行呈递。(病毒感染细胞合成病毒蛋白、肿瘤细胞合成肿瘤蛋白、吞噬体中逃逸至细胞质中的抗原、ER中折叠错误的自身蛋白) 抗原肽-MHCI复合物的形成 第一步 内源性抗原降解成抗原肽 胞质内的靶蛋白和泛素结合,被蛋白酶体的帽子结构识别,被剪切成多肽 蛋白酶体为中空圆柱体结构,分为具有酶活性的两个
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  232. <a href="/1747.html" target="_self">
  233. 实用免疫学(七)适应性免疫:体液免疫
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  238. 环境中的病原体侵入生物机体后,胞外菌寄居在宿主的细胞外组织液、淋巴液和血液等体液中。侵入的病原体会刺激特异性B细胞活化并分化为浆细胞。根据B细胞对Ag的反应,将Ag分为TI-Ag(胸腺非依赖性抗原)和TD-Ag(胸腺依赖性抗原)。活化的B细胞通过产生抗体来发挥效应。 TI-Ag该类抗原刺激机体产生抗体无需T细胞的辅助,可以分为TI-1Ag和TI-2Ag。 TI-1Ag 既有抗原表位又有丝裂原性
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  262. <a href="/1738.html" target="_self">
  263. 实用免疫学(八)适应性免疫番外篇一:抗原
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  268. 适应性免疫的激活离不开抗原。抗原是能被TCR和BCR特异性识别,促使抗原特异性T、B细胞活化、增殖和分化,产生免疫应答效应产物,并与之结合,进而发挥适应性免疫应答效应的物质。其有两个重要且独立的特性:免疫原性和抗原性(免疫反应性)。 免疫原性:诱导适应性免疫应答的能力 抗原性:与免疫效应产物结合的能力 不具有免疫原性的小分子半抗原可以是大分子蛋白质载体共价结合获得免疫原性。(青霉素与血浆蛋白、
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  293. 实用免疫学(五)适应性免疫:细胞免疫一 Th细胞
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  298. 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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  304. <time datetime="2022-02-23 00:56" pubdate>
  305. 2022-02-23
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  321. <h2 class="index-header">
  322. <a href="/1713.html" target="_self">
  323. 实用免疫学(四)从固有免疫到适应性免疫
  324. </a>
  325. </h2>
  326. <a class="index-excerpt index-excerpt__noimg" href="/1713.html" target="_self">
  327. <div>
  328. 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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  352. <a href="/1704.html" target="_self">
  353. 实用免疫学(三)固有免疫番外篇一:补体系统
  354. </a>
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  356. <a class="index-excerpt index-excerpt__noimg" href="/1704.html" target="_self">
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  358. 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&#x2F;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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  381. <h2 class="index-header">
  382. <a href="/1699.html" target="_self">
  383. 实用免疫学(二)固有免疫应答
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  385. </h2>
  386. <a class="index-excerpt index-excerpt__noimg" href="/1699.html" target="_self">
  387. <div>
  388. 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&#x2F;C3a可直接作用于肥大细胞,释放炎性介质
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