消化系统疾病

中国医学文摘·内科学1998年第19卷第5期.469·,83422间皮细胞在腹膜抗菌防御中的作用/减燕…//中华内科杂志一1998,37(3)一158~161 对大鼠的观察表明,腹膜间皮细胞粘附分子一1(ICAM一1),用细菌脂多糖(LPS)、金葡菌肠毒素和IL一l刺激培养6小时可增加间皮细胞ICAM一1的表达,同时可增加细菌对间皮细胞的粘附率。单核细胞对粘附间皮细胞表面的调理与未调理细菌均能很好地吞噬,两者吞噬率比较无明显差异。认为ICAM一1的表达增加,为单核细胞吞噬粘附其表面的细菌提供了一个适宜的环境,主动参与腹膜炎反应过程,在腹膜抗菌防御中起重要作用…     

地塞米松对细胞因子刺激的人眼球后成纤维细胞的影响

目的 探讨地塞米松治疗Ｇｒａｖｅｓ眼病（ＧＯ）的作用机制。方法 应用细胞培养技术，测定加入细胞因子及地塞米松后细胞间粘附分子－１（ＩＣＡＭ－１）表达和ＤＮＡ合成情况。结果 肿瘤坏死因子（ＴＮＭＦ）－α（１０＾Ｕ／ｍｌ）、干扰素（ＩＮＦ）－γ（１００Ｕ／ｍｌ）和白细胞介素（ＩＬ）－１β（１００Ｕ／ｍｌ）均能强烈刺激眼球后成纤维细胞表面ＩＣＡＭ－１表达，而地塞米松能明显地抑制这种刺激作用，但所需浓度及     

细胞间粘附分子—1在肝病中的表达

细胞间粘附分子－１（ＩＣＡＭ－１）在炎症细胞因子刺激下，在病毒性肝炎、酒精性肝病、肝细胞癌（ＨＣＣ）和自身免疫性肝病中表达水平明显增高，其表达程度与炎症程度呈正相关，与肝组织病变及病变组织学分级均有关；ＩＣＡＭ－１表达水平的高低可能影响干扰素对慢性病毒性肝炎的治疗；ＩＣＡＭ－１表达与肿瘤的大小、进展、转移也有关。并随病情的缓解而下降。促进ＩＣＡＭ－１表达的细胞因子有ＩＦＮ－γ、ＴＮＦ－α、ＩＬ－１     

脂多糖致肺血管内巨噬细胞形态和功能的改变

目的探讨肺血管内巨噬细胞（ＰＩＭ）在感染性急性肺损伤（ＡＬＩ）发病中的作用。方法仿Ｍｏｒｔｏｎ法灌洗肺血管床，贴壁法分离猪ＰＩＭ，并用光镜、电镜观察鉴定；胸腺细胞增殖法测脂多糖（ＬＰＳ）刺激前后ＰＩＭ培养上清白细胞介素１β（ＩＬ－１β）活性，酶联免疫吸附试验（ＥＬＩＳＡ）法测肿瘤坏死因子α（ＴＮＦ－α）、白细胞介素６（ＩＬ－６）、白细胞介素８（ＩＬ－８）含量。结果刺激后的ＰＩＭ伪足增长、增多，溶酶体和吞噬体亦增多；释放ＴＮＦα、ＩＬ－１β、ＩＬ－６、ＩＬ－８增多，峰值分别出现在刺激后的１ｈ、２ｈ、４ｈ和６ｈ。与刺激前相比，Ｐ＜０．０１。结论改良的Ｍｏｒｔｏｎ法能成功分离猪ＰＩＭ；ＬＰＳ刺激后的ＰＩＭ吞噬分泌功能活跃，其中ＴＮＦα、ＩＬ－１β升高最早，提示其在ＡＬＩ发病早期起重要作用；而ＩＬ－６、ＩＬ－８升高较晚，可能在ＡＬＩ发病后期起重要作用     

Octreotide治疗Graves'眼病机理探讨

目的　探讨Ｏｃｔｒｅｏｔｉｄｅ 对细胞因子刺激后的人眼球后成纤维细胞的细胞间粘附分子１（ＩＣＡＭ１） 表达及ＤＮＡ 合成的影响。方法　应用细胞培养技术, 测定加入细胞因子及Ｏｃｔｒｅｏｔｉｄｅ后ＩＣＡＭ１ 表达和ＤＮＡ 合成情况。结果　ＴＮＦα（１０３ Ｕ／ｍｌ） 、γＩＮＦ（１００ Ｕ／ｍｌ） 和ＩＬ１β（１００ Ｕ／ｍｌ） 均能强烈刺激眼球后成纤维细胞表面ＩＣＡＭ１ 表达,而低浓度（ 即药理浓度）Ｏｃｔｒｅｏｔｉｄｅ 能明显地抑制这种刺激作用,但所需浓度及发挥抑制作用的时间各不相同;同样,低浓度Ｏｃｔｒｅｏｔｉｄｅ 也能抑制细胞因子（除ＩＬ１β外） 刺激的ＤＮＡ 合成。结论　Ｏｃｔｒｅｏｔｉｄｅ 治疗Ｇｒａｖｅｓ’眼病的作用途径部分是通过抑制细胞因子的作用,使ＩＣＡＭ１ 表达及ＤＮＡ 合成减少,它可能具有免疫调节的特性。     

坏死性胰腺炎对时某些粘附分子表达对中性粒细胞在肺脏聚集的影响

目的 探讨急性出血坏死性胰腺炎（ＡＮＰ）时中性粒细胞（ＰＭＮ）聚集了肺脏的机制。方法 在ＡＮＰ并发急性肺损伤（ＡＬＩ）模型，采用免疫组化技术等方法，动态观察ＡＮＰ后大鼠肺脏实质细胞细胞间粘附分子－１（ＩＣＡＭ－１）、ＰＭＮ表面巨噬细胞分化抗原－１（ＣＤ１１ｂ／ＣＤ１８）的表达改变和ＰＭＮ肺脏聚集的变化。结果 ＡＮＰ的肺脏ＩＣＡＭ－１表达逐渐增加，与ＰＭＮ肺脏聚集程度呈显著正相关，而ＰＭＮ表面ＣＤ１     

培哚普利和洛沙坦对心肌细胞间粘附分子-1表达的影响

目的：研究血管紧张素转换酶抑制剂（ＡＣＥＩ）培哚普利和血管紧张素Ⅱ的Ⅰ型受体（ＡＴ１）拮抗剂洛沙坦对肿瘤坏死因子（ＴＮＦ）α刺激的心肌细胞间粘附分子－１（ＩＣＡＭ－１）表达的影响。　　方法：运用流式细胞仪观察培养的乳鼠心肌细胞ＩＣＡＭ－１的表达量。　　结果：ＴＮＦ－α可明显增加心肌细胞ＩＣＡＭ－１的表达量。从时间变化看,以刺激６ 小时表达量最高,但随作用时间延长表达量减少。培哚普利（１０－ ６ ｍ ｏｌ／Ｌ,１０－ ８ ｍ ｏｌ／Ｌ）和洛沙坦（１０－ ６ ｍ ｏｌ／Ｌ,１０－ ８ ｍ ｏｌ／Ｌ）均可明显抑制ＴＮＦ－α刺激的心肌细胞ＩＣＡＭ－１ 的表达量。　　结论：培哚普利和洛沙坦均可抑制培养的心肌细胞因子ＴＮＦ－α诱导而上调的ＩＣＡＭ－１ 的表达,这可能是ＡＣＥＩ和ＡＴ１受体拮抗剂治疗心力衰竭时的心脏保护效应的重要原因     

细胞间粘附分子1mRNA在哮喘豚鼠支气管组织中的原位表达

为了解哮喘豚鼠支气管组织中的细胞间粘附分子１（ＩＣＡＭ－１）ｍＲＮＡ表达情况，将实验豚鼠随机分为正常对照组、氟美松组和哮喘组，采用原位杂交方法显示ＩＣＡＭ－１ｍＲＮＡ的表达变化，用ＨＥ染色方法来测定炎细胞在支气管粘膜中的浸润程度。原位杂交结果显示，ＩＣＡＭ－１ｍＲＮＡ主要在支气管粘膜下的小血管、毛细血管内皮细胞以及支气管上皮细胞的胞浆内表达。定量分析结果表明，哮喘组豚鼠支气管组织表达ＩＣＡＭ－１ｍＲＮＡ较正常对照组及氟美松组显著增加（Ｐ＜０．０２，Ｐ＜０．０５），哮喘豚鼠支气管组织ＩＣＡＭ－１ｍＲＮＡ的表达量与炎细胞总数之间显著相关（Ｐ＜０．０５）。提示支气管粘膜组织ＩＣＡＭ－１ｍＲＮＡ表达与哮喘支气管粘膜嗜酸细胞为主的炎细胞浸润有关，糖皮质激素能够抑制细胞粘附分子的表达。     

健康人细胞间粘附分子-1血浆水平与心肌梗塞危险

细胞间粘附分子－１（ＩＣＡＭ－１）介导白细胞向血管内皮壁的移行和粘附,据认为后者是动脉粥样硬化发生和发展的关键性步骤。但目前健康以后患急性心肌梗塞（ＡＭＩ）的健康人血浆中可溶性ＩＣＡＭ－１（ｓＩＣＡＭ－１）是否升高尚不清楚。本文对大宗人群进行了前瞻性...     

高血压病人白细胞流变性与细胞粘附分子表达的变化

目的探讨白细胞流变性和细胞粘附分子（ＣＡＭＳ）表达与高血压发生及病情严重程度的关系。方法采用红细胞变形能力测定仪、体外血栓血小板粘附两用仪和酶联免疫吸附法（ＥＬＩＳＡ），检测１４９例高血压病人和１１０例健康人外周血白细胞变形能力（ＬＤ）、白细胞粘附功能（ＬＡＦ）、白细胞ＣＤ１８表达及血清可溶性细胞间粘附分子－１（ｓＩＣＡＭ－１）浓度的变化。结果高血压病人白细胞滤过指数（ＬＦＩ）、白细胞粘附率（ＬＡＲ）、白细胞ＣＤ１８表达和ｓＩＣＡＭ－１浓度均明显增高，与对照组比较差异有极显著性（Ｐ＜０．００１），三期病人各指标之间比较差异也具有极显著性（Ｐ＜０．００１），且以第３期病人各指标增高最明显。高血压病人ＬＡＲ与ＬＦＩ呈正相关（ｒ＝０．５７９，Ｐ＜０．００１）；ＬＡＲ和ＬＦＩ与白细胞ＣＤ１８表达和ｓＩＣＡＭ－１浓度呈正相关（ｒ＝０．６６２～０．８０４，Ｐ＜０．００１）。结论ＬＤ降低、ＬＡＦ及白细胞ＣＤ１８表达和ｓＩＣＡＭ－１浓度增高参与高血压的发生，且与病情严重程度有密切关系。     

肾小球系膜细胞白细胞介素-6基因表达与白细胞介素-13的关系

目的探讨白细胞介素-13(IL-13)对于体外培养大鼠系膜细胞白细胞介素-6(IL-6)分泌及其基因表达的影响,以研究IL-13对肾小球疾病状态下肾脏系膜细胞炎症反应的抑制作用。方法用酶联免疫吸附法(ELISA)测定系膜细胞IL-6分泌量,用逆转录聚合酶链反应(RT-PCR)检测系膜细胞IL-6mRNA表达。结果正常培养条件下系膜细胞IL-6mRNA表达及IL-6分泌水平较低,脂多糖(LPS)可刺激系膜细胞IL-6mRNA的表达及IL-6分泌水平,而IL-13则呈剂量依赖性地抑制LPS诱导的系膜细胞IL-6分泌及其mRNA表达。结论IL-13抑制LPS诱导的体外培养的系膜细胞IL-6产生,故可能对于肾小球疾病状态下肾脏的系膜细胞炎症反应具有抑制作用。     

Impaired interleukin-1beta expression by monocytes stimulated with Staphylococcus aureus in diabetes

Diabetic patients with poorly controlled blood glucose have frequent and persistent bacterial infections particularly those infecting the skin, such as Staphylococcus aureus and S. epidermidis. The function of phagocytes of diabetic patients is believed to be impaired due to hyperglycemia, leading to suboptimal immune response to clear acute infection. The present study investigated interleukin (IL)-1beta expression by diabetic patients' monocytes (n = 22) experimentally infected with S. aureus compared with that from healthy subjects (n = 30). In addition, the in vitro effect of hyperglycemia on IL-1beta expression by monocytes from normal subjects (n = 18) stimulated with S. aureus and S. epidermidis was investigated. Monocytes from diabetic patients, stimulated or not with S. aureus, express significantly lower levels of IL-1beta than those from healthy subjects. In vitro hyperglycemia did not affect IL-1beta expression by unstimulated monocytes. However, at the same levels of glucose normal monocytes stimulated with S. aureus produce significantly higher IL-1beta than those stimulated with S. epidermidis. These findings suggest that diabetic patients have abnormally lower IL-1beta expression and hyperglycemia is related to abnormal expression of IL-1beta by monocytes, which could lead to enhanced susceptibility to infection by the more virulent bacteria.     

Polar production of interleukin-8 by mesothelial cells promotes the transmesothelial migration of neutrophils: role of intercellular adhesion molecule-1

Migration of polymorphonuclear neutrophils (PMNL) from the vascular compartment into the pleural space occurs rapidly during the development of parapneumonic effusions. This study investigated the polarized secretion of interleukin (IL)-8 in activated pleural mesothelial cells (PMC) and the migration of PMNL across resting, activated PMC monolayers. Results show that PMC produce IL-8 in a polar manner. When PMC were stimulated with Staphylococcus aureus or IL-1beta at the basal or at the apical surface, significantly (P< .05) more IL-8 was released toward the apical surface. This polarized production of IL-8 was confirmed by in situ hybridization. PMNL migration was higher from the basilar to apical than from the apical to basilar surface of PMC. Neutralizing antibodies against IL-8 and intercellular adhesion molecule (ICAM)-1 significantly (P< .001) blocked PMNL migration across activated monolayers. Thus, during pleural inflammation, PMC regulate the influx of PMNL into the pleural space by polar production of IL-8 and expression of ICAM-1.     

Adherence of peritonitis-causing staphylococci to human peritoneal mesothelial cell monolayers

The adherence of staphylococci to monolayers of human mesothelial cells was studied. Adherence of Staphylococcus aureus to mesothelial cell monolayers was 3.4-fold better than to plastic (P less than .01) whereas that of Staphylococcus epidermidis was 3.0-fold less than to plastic (P less than .01). Neither serum albumin nor gelatin inhibited staphylococcal binding. S. aureus adherence correlated with the amount of cell wall protein A (r = .63, P less than .05) but not with fibronectin binding; it was significantly inhibited by the addition of purified cell wall lipoteichoic acid (55% +/- 2.7%), teichoic acid (34.5% +/- 3.4%), and protein A (25.6% +/- 2.9%) but not peptidoglycan. Protein A- and teichoic acid-deficient mutants adhered less well than their parent strains, and encapsulated S. epidermidis adhere well to human monothelial cells. Staphylococcal binding may involve cell wall lipoteichoic acid, teichoic acid, and protein A.     

高浓度胰岛素对人树突状细胞分化、成熟及免疫功能的影响

目的:研究高浓度胰岛素对树突状细胞(Dendritic Cell,DC)分化、成熟及免疫功能的影响。方法:采用连续贴壁法分离正常人外周血单核细胞,在含重组人粒-巨噬细胞集落刺激因子(GM-CSF,100ng/ml)和重组人白细胞介素-4(IL-4,100ng/ml)的完全培养基中培养。5天后收集细胞,重新铺板后继续在胰岛素浓度分别为0nmol/L、10nmol/L及100nmol/L的培养基中培养48小时,收集细胞和上清液,采用流式细胞术检测细胞表面CD40、CD80和CD83的表达;用ELISA法检测上清液中细胞因子IL-12、IL-10、TNF-α的浓度;用倒置显微镜动态观察DC形态变化。结果:胰岛素浓度为10nmol/L、100nmol/L组的DC表面标成CD40、CD80和CD83阳性表达率较含胰岛素0nmol/L的对照组升高,培养上清液中细胞因子IL-12、TNF-α的浓度也较对照组升高,而细胞因子IL-10的浓度则较对照组降低。结论:高浓度胰岛素促进了树突状细胞表型CD40、CD80和CD83的表达;促进了DC对细胞因子IL-12和TNF-α的分泌;对IL-10的分泌则起抑制作用。高浓度胰岛素通过促进树突状细胞免疫功能的成熟,可能是其参与动脉粥样硬化免疫炎症反应的发生、发展的机制之一。     

Differential modulation of the induction of inflammatory mediators by antibiotics in mouse macrophages in response to viable Gram-positive and Gram-negative bacteria

We have investigated effects of beta-lactam antibiotics on TNF-alpha, and iNOS production from mouse peritoneal macrophages following co-culture with Escherichia coli or Staphylococcus aureus bacteria. Ceftazidime and aztreonam enhanced TNF-alpha secretion from macrophages stimulated with E. coli; however, imipenem does not alter either the kinetics or magnitude of TNF-alpha in E. coli-treated macrophages. Similar treatments with S. aureus co-cultured with macrophages markedly altered profiles of TNF-alpha response characterized by apparent early TNF-alpha peak relative to untreated S. aureus. All antibiotics increased E. coli-induced iNOS expression as assessed by both mRNA and protein. These same antibiotics significantly reduced S. aureus-induced iNOS levels of RNA. Both ceftazidime and aztreonam enhanced LPS release from E. coli in comparison to low-level LPS release from imipenem-treated bacteria, consistent with observed differences in TNF-alpha release. Incubation of all three antibiotics with S. aureus similarly increased levels of the cell wall constituent protein A detected in supernatants at early time points indicating microbial lysis. In parallel, S. aureus culture supernatants from 2-h incubation with antibiotics enhanced TNF-alpha release. These results indicate that different cellular mechanisms contribute to antibiotic-mediated regulation of TNF-alpha and iNOS secretion in mouse macrophages in response to E. coli versus S. aureus.     

卡巴胆碱对脂多糖刺激后人血单核细胞和淋巴细胞免疫功能的影响

目的探讨拟胆碱药物卡巴胆碱对脂多糖（LPS）刺激后单核细胞人类白细胞组织相容性抗原-DR（HLA-DR）表达率及淋巴细胞凋亡率的影响。方法分离、培养正常人外周血单核细胞和淋巴细胞，对照组仅加1640培养液，LPS组加LPS刺激，LPS＋卡巴胆碱组先用不同浓度卡巴胆碱（100、10、1、0．1、0．01μmol／L）预处理细胞后，再加入LPS（100μg／L）刺激，培养12h后用流式细胞术检测CD14＋单核细胞HLA-DR表达率和外周血淋巴细胞凋亡率。结果LPS单独刺激单核细胞时，其HLA-DR表达率明显降低，用卡巴胆碱预处理后，HLA—DR表达率随着卡巴胆碱浓度的增高而增高。LPS单独刺激淋巴细胞时，淋巴细胞凋亡率明显增加，而用卡巴胆碱预处理后，淋巴细胞凋亡率随着卡巴胆碱浓度的增高而降低。结论卡巴胆碱对LPS引起的人血单核细胞和淋巴细胞免疫功能下调有显著抑制作用。     

Lactic acid bacteria secrete metabolites retaining anti-inflammatory properties after intestinal transport

BACKGROUND: Probiotic bacteria have a beneficial effect on intestinal inflammation. In this study, we have examined the effect of lactic acid and commensal Gram positive (+) bacteria conditioned media (CM) on tumour necrosis factor alpha (TNF-alpha) release and the mechanisms involved. METHODS: Lipopolysaccharide (LPS) induced TNF-alpha secretion by peripheral blood mononuclear cells or the THP-1 cell line was monitored in the presence or absence of bacteria CM obtained from two probiotic strains, Bifidobacterium breve (Bb) and Streptococcus thermophilus (St), and three commensal bacterial strains (Bifidobacterium bifidum, Ruminococcus gnavus, and unidentified Streptococcus). Bb and St bacteria CM were allowed to cross filter grown intestinal epithelial cell monolayers (HT29-19A) to assess intestinal transport of active bacterial products. These products were characterised and their effect on LPS binding to THP-1 cells and nuclear factor kappa B (NF kappa B) activation assessed. RESULTS: Dose dependent inhibition of LPS induced TNF-alpha secretion was noted for both probiotic bacteria CM (64% and 71% inhibition for Bb and St, respectively) and to a lesser extent commensal bacteria CM (21-32% inhibition). Active products from Bb and St were resistant to digestive enzymes and had a molecular mass <3000 Da. Their inhibitory effect was preserved after transepithelial transport across intestinal cell monolayers, mainly in inflammatory conditions. LPS-FITC binding to THP-1 cells and NF kappa B activation were significantly inhibited by Bb and St CM. CONCLUSION: B breve and S thermophilus release metabolites exerting an anti-TNF-alpha effect capable of crossing the intestinal barrier. Commensal bacteria also display a TNF-alpha inhibitory capacity but to a lesser extent. These results underline the beneficial effect of commensal bacteria in intestinal homeostasis and may explain the role of some probiotic bacteria in alleviating digestive inflammation.     

Interleukin‐18 enhances monocyte tumor necrosis factor α and interleukin‐1β production induced by direct contact with T lymphocytes: Implications in rheumatoid arthritis

Objective

At sites of inflammation, T cells exert pathologic effects through direct contact with monocyte/macrophages, inducing massive up‐regulation of interleukin‐1 (IL‐1) and tumor necrosis factor α (TNFα). We examined the regulatory effects of IL‐18 on monocyte activation by direct contact with T lymphocytes in rheumatoid arthritis (RA).

Methods

Activated T cells were isolated from RA synovial fluid. Resting T cells and monocytes were isolated from peripheral blood mononuclear cells. RA synovial T cells or phytohemagglutinin (PHA)–stimulated T cells were fixed by paraformaldehyde and then cocultured with monocytes at a ratio of 4:1. Levels of TNFα, IL‐1β, IL‐10, and IL‐18 were measured by enzyme‐linked immunosorbent assay. Expression of adhesion molecules, IL‐18 receptor, and TNF receptors was analyzed by flow cytometry. Expression of NF‐κB p65, phosphorylated IκBα, and phosphatidylinositol 3‐kinase (PI 3‐kinase) p110 was analyzed by Western blotting.

Results

IL‐18 dose‐dependently enhanced the production of IL‐1β and TNFα, but not IL‐10, by monocytes following contact with RA synovial T cells or PHA‐prestimulated T cells. NF‐κB inhibitors N‐acetyl‐L ‐cysteine and Bay 11‐7085 and PI 3‐kinase inhibitor LY294002 inhibited the enhancing effects of IL‐18, but MAPK p38 inhibitor SB203580, ERK inhibitor PD98059, and JNK inhibitor SP600125 did not. Increased levels of NF‐κB in the nucleus, phosphorylated IκB, and PI 3‐kinase were confirmed in monocytes cocultured with PHA‐prestimulated T cells, and the levels were further increased by stimulation with IL‐18. Neutralizing antibody to IL‐18 inhibited monocyte activation induced by direct contact with PHA‐prestimulated T cells. Via cell–cell contact, PHA‐prestimulated T cells increased autocrine production of IL‐18 by monocytes, which was mediated by activation of the NF‐κB and PI 3‐kinase pathways, and up‐regulated the expression of the IL‐18 receptor in monocytes. IL‐18 up‐regulated the expression of the TNF receptors vascular cell adhesion molecule 1 (VCAM‐1) and intercellular adhesion molecule 1 (ICAM‐1) on monocytes. Blocking the binding of the TNF receptors VCAM‐1 or ICAM‐1 on monocytes to their ligands on stimulated T cells suppressed the IL‐18–enhanced production of TNFα and IL‐1β in monocytes induced by contact with PHA‐prestimulated T cells.

Conclusion

IL‐18 augments monocyte activation induced by contact with activated T cells in RA synovitis, which is dependent on activation of the NF‐κB and PI 3‐kinase pathways. IL‐18 up‐regulates the expression of the TNF receptors VCAM‐1 and ICAM‐1 on monocytes, which mediate the enhancing effects of IL‐18 on T cell–monocyte contact.

     

HepG2.2.15细胞诱导MT2淋巴细胞凋亡及其意义

观测表达Ｆａｓ抗原（Ｆａｓ）的Ｔ淋巴细胞一感染乙型肝炎病毒的ＭＴｓ细胞对表达Ｆａｓ配体（ＦａｓＬ）的实质细胞一ＨｅｐＧ２２．１５细胞的敏感性,了解乙型肝炎病毒感染对淋巴细胞和肝实质细胞交互作用的影响。方法体外培养ＭＴ２细胞,用乙型肝炎病毒诱导表达ＦａｓＬ。将表达ＦａｓＬ的ＨｅｐＧ２．２．１５细胞与其共孵育后,以Ｔｕｎｅｌ法观测ＭＴ２细胞凋亡情况。结果ＭＴ２细胞感染乙型肝炎病毒后可测到Ｆａｓ表达信号。与表达ＦａｓＬ的ＨｅＰＧ２．２．１５细胞共孵育４８～７２小时以后,出现凋亡信号。结论乙型肝炎病毒诱导表达Ｆａｓ的ＭＴｓ细胞与表达ＦａｓＬ的ＨｅｐＧ２．２．１５细胞交互作用后发生凋亡,表明通常在乙型肝炎发病中作为效应细胞的淋巴细胞,亦可成为凋亡靶细胞。