出版年:

研究生:

謝沛諭

研究生(英文姓名):

論文名稱:

肺部CD4-CD8-雙陰性T細胞在過敏性發炎反應及病毒感染的角色

英文論文名稱:

Pulmonary CD4-CD8-Double-Negative T Cells In Allergic Inflammation And Viral Infection

指導教授:

余俊強

學位類別:

碩士

校院名稱:

國立成功大學　

系所名稱:

微生物及免疫學研究所

學年度:

85

語文別:

中文

論文頁數:

46

關鍵詞:

家塵虫滿 ; 嗜酸性球發炎

英文關鍵詞:

Dermatophagoides farinnad

被引用次數:

0

[ 摘要 ]

　　在小鼠的肺臟細胞中，已經知道有一群不帶有CD4及CD8表面標記的T細胞。這群細胞存在的意義及功能，目前知道的非常的少。我們嘗試以細胞流體分析儀偵測正常BALB/c小鼠肺藏單核細胞中細胞標記，確實發現有CD4-CD8- double-negative (DN)T細胞存在於肺間質及支氣管肺泡衝洗液中，兩者的CD3+CD4-8-佔其中單核細胞的6.9-8.3%，TCRαβ+CD4-8-佔5.1-6.9%，而TCRγδCD4-8-細胞較少只佔1.4-2.1%。
　　以家塵□（Dermatophagoides farinnae, Der f）激發致敏小鼠所誘發的嗜酸性球發炎反應的動物模式中，CD4-8-T細胞於激發後第三天，在支氣管肺泡沖液及肺間質中都有明顯的增加，利用補體媒介細胞毒殺方式去除CD4+和CD8+，再利用免疫磁性抗體珠選取DNT細胞，結果發現激發後第二天肺臟的DNT細胞可表現IL-10及IL-5的mRNA。
　　以呼吸道融合病毒感染小鼠會誘發急性（第二天）嗜中性球及慢性（第五天）淋巴球浸潤。其中CD8+及CD4-8-T細胞也明顯增加，尤其CD4-8-T細胞的出現時間有biphase現象，第一個高峰在感染後第二天，另一個高峰在第七天，我們推測CD4-CD8-DNT細胞可能與抑制免疫反應和發炎反應有關。

[ 英文摘要 ]

　　A distince subpopulation of T cells bearing neither CD4 nor CD8 molecules (CD4-CD8-)have been dentified in the lung as well as other non-lymphoid tissues. Using flow cytometric analysis, we demonstrated that CD4-CD8- T cells were present in both bronchoalveolar lavage and lung parenchyma of normal BALB/c mice. In addition, in a dust mite (Dermatophagoides farnae, Der f) induced asthma model, which is characterized by a T-cell-dependent, IL-5-mediated eosinophilic inflammation, we have observed a significant increased in CD4-CD8-T cells in the airways of sensitized mice after challenge. CD4-CD8- T cells were then enriched from lung tissue by depletion of CD4+ and CD8+ T cells through complement-mediated lysis using mAbs to CD4 and CD8 for further characterization. RT-PCR analysis showed that CD4-CD8-T cells derived from sensitized mice expressed mRNA for IL-5 and IL-10 after challenge.
　　Primary respiratory syncytial virus infection of mice produced an acute influx of neutrophils following with a chronic lymphocytic infltration at day 2 and day 7, respectially. Both CD8+ and CD4-CD8- T cells were significantly increased. Furthermore, the CD4-CD8-T cells had a biphase pattern with a peak at day 2 and a secondary peak at day 7 afte infection. The time course of the enhanced expansion of CD4-CD8-T cells was closed associated with the onset and development of virus-induced inflammation. Taken together, we speculate that CD4-CD8-T cells might play a role in down-regulating immune as well as inflammatory responses.