Antiviral CD8+ T cell effector activities in situ are regulated by target cell type.
Antiviral CD8+ T cell effector activities in situ are regulated by target cell type.
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DOI：
10.1084/jem.20101850
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发表时间：
2011-01-17
期刊：
影响因子：
--
通讯作者：
Braciale TJ
中科院分区：
文献类型：
--
作者：
Hufford MM;Kim TS;Sun J;Braciale TJ
在感染流感的小鼠的肺中，细胞毒性T淋巴细胞的活性受到所遇到的靶细胞类型的调节。细胞毒性T淋巴细胞（CTL）通过其介导受感染细胞的接触依赖性裂解和释放可溶性促炎细胞因子和趋化因子的能力在病毒感染的解决中发挥突出作用。在体内感染部位控制这些抗病毒效应物活性的因素尚不清楚。使用流感感染的小鼠模型，我们观察到受感染的肺中CTL效应活性的表达由所遇到的靶细胞类型决定。CD45+肺浸润炎性单核细胞，特别是CD11chi树突状细胞，触发CTL细胞毒性和炎症介质的释放，而CD45−流感感染的呼吸道上皮细胞仅刺激CTL细胞毒性。CTL促炎介质的释放由CD45+炎性细胞表达的共刺激配体（CD80和CD86）调节。这些研究结果表明，新的机制控制CTL效应活性，并有潜在的重要意义，控制过度的肺部炎症和免疫病理学，同时保持最佳的病毒清除呼吸道病毒感染。
In the lungs of mice infected with influenza, the activity of cytotoxic T lymphocytes is modulated by the type of target cell encountered. Cytotoxic T lymphocytes (CTLs) play a prominent role in the resolution of viral infections through their capacity both to mediate contact-dependent lysis of infected cells and to release soluble proinflammatory cytokines and chemokines. The factors controlling these antiviral effector activities in vivo at infection sites are ill defined. Using a mouse model of influenza infection, we observed that the expression of CTL effector activity in the infected lungs is dictated by the target cell type encountered. CD45+ lung infiltrating inflammatory mononuclear cells, particularly CD11chi dendritic cells, trigger both CTL cytotoxicity and release of inflammatory mediators, whereas CD45− influenza-infected respiratory epithelial cells stimulate only CTL cytotoxicity. CTL proinflammatory mediator release is modulated by co-stimulatory ligands (CD80 and CD86) expressed by the CD45+ inflammatory cells. These findings suggest novel mechanisms of control of CTL effector activity and have potentially important implications for the control of excess pulmonary inflammation and immunopathology while preserving optimal viral clearance during respiratory virus infections.
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影响因子：
15.3
作者：
Lukacher, A E;Braciale, V L;Braciale, T J
通讯作者：
Braciale, T J
影响因子：
4.4
作者：
Liu, F;Whitton, JL
通讯作者：
Whitton, JL
影响因子：
2.2
作者：
Lutz, MB;Kukutsch, N;Schuler, G
通讯作者：
Schuler, G
影响因子：
5.4
作者：
Hao, Xueli;Kim, Taeg S.;Braciale, Thomas J.
通讯作者：
Braciale, Thomas J.
影响因子：
5.4
作者：
HOU, S;DOHERTY, PC
通讯作者：
DOHERTY, PC