炎癥與免疫研究進(jìn)展唐宏

炎癥與免疫研究進(jìn)展唐宏中科院感染免疫重點(diǎn)實(shí)驗(yàn)室炎癥的病理特征與進(jìn)程炎癥的局部臨床特征是紅、熱、腫、痛和組織/器官功能衰竭紅熱:炎癥局部血管擴(kuò)張、血流加快所致。腫脹:局部炎癥性充血、血液成分滲出引起。疼痛:滲出物壓迫和炎癥介質(zhì)直接作用于神經(jīng)末梢而引起疼痛。功能衰竭：基于炎癥的部位、性質(zhì)和嚴(yán)重程度將引起不同的功能障礙，如肺炎影響氣血交換從而引起缺氧和呼吸困難/窘迫等。炎癥通常可按其病程分為急性炎癥和慢性炎癥急性炎癥：啟動(dòng)急驟，持續(xù)幾天至一個(gè)月。有害刺激一旦去除，炎癥也就隨之消失。以血漿滲出和中性粒細(xì)胞浸潤為主要特征。慢性炎癥：持續(xù)數(shù)月至數(shù)年，以淋巴細(xì)胞和單核-巨噬細(xì)胞浸潤以及微/小血管和結(jié)締組織增生為主要病理學(xué)特征。炎癥的細(xì)胞反應(yīng)1、吞噬細(xì)胞是啟動(dòng)炎癥反應(yīng)的重要效應(yīng)細(xì)胞，包括巨噬細(xì)胞和中性粒細(xì)胞。吞噬細(xì)胞通過其表面表達(dá)的多種受體(甘露糖受體，葡聚糖受體，Toll樣受體等)，迅速識(shí)別并攝入外源微生物，形成吞噬體，繼而與溶酶體結(jié)合形成吞噬溶酶體，微生物通過氧依賴或氧非依賴途徑被殺傷。被激活的吞噬細(xì)胞同時(shí)分泌大量的促炎癥因子和趨化因子（IL-1，TNF，IL-6和KC/CXCL8等)，發(fā)揮多種非特異性效應(yīng)，包括致炎，致熱，趨化炎癥細(xì)胞，激活免疫細(xì)胞，抑制病毒復(fù)制，胞毒作用等。中性粒細(xì)胞存在于外周血，壽命短，數(shù)量多；巨噬細(xì)胞是從血液中的單核細(xì)胞分化而來分布于不同組織中，壽命長，形體大，富含細(xì)胞器。2、NK細(xì)胞也是參與炎癥反應(yīng)的重要細(xì)胞，在多種細(xì)胞因子刺激下，殺傷感染細(xì)胞內(nèi)的微生物并產(chǎn)生細(xì)胞因子，進(jìn)一步促進(jìn)炎癥細(xì)胞發(fā)揮作用而產(chǎn)生級(jí)聯(lián)放大效應(yīng)。3、此外，DC、γδT、B1、肥大細(xì)胞、NKT、上皮細(xì)胞等在一定范圍內(nèi)參與炎癥反應(yīng)。炎癥是所有具有血管系統(tǒng)的個(gè)體，其組織與細(xì)胞對(duì)損傷性因子/因素所產(chǎn)生的反應(yīng)PAMPvsDAMPDongetal,NatMed(2007)AdaptiveimmunesystempreventsoverreactiveinnateimmunityintheinitialphaseofinfectionsA02040608010002468101214Balb/cNudeDaysafterinjection%survivalBCBalb/cNude23456Day2Day4LogPFU/gmLiverTNF-

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