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Nature Medicine:效应T细胞产生IL-10控制病毒性肺炎

来源:医学空间 2009-03-01 20:28

《自然医学》杂志刊登了弗吉尼亚大学免疫中心的报道,在急性病毒感染灶周围发现CD8(+)和CD4(+)效应T细胞,其具有抗炎作用。

激活的抗原特异性T细胞可产生的各种效应分子,在清除感染的同时,还可能产生炎症和组织损伤。

研究者发现,在急性流感病毒感染者肺部生成大量IL-10,这大部分是由病毒特异性T细胞、CD8(+)T细胞产生。这些T细胞周边同时产生IL-10及致炎因子,同时1型辅助T或1型细胞毒性T细胞特征。值得注意的是,抑制T细胞源性IL-10将加重肺部炎症,导致致死性伤害。

研究表明,T细胞抗病毒时发挥监督职能,即通过产生抗炎细胞因子,调节流感感染引起的肺部炎症和损伤程度。这项研究对高致病性流感病毒感染有潜在的基础价值。(生物谷Bioon.com)

生物谷推荐原始出处:

Nature Medicine 22 February 2009 | doi:10.1038/nm.1929

Effector T cells control lung inflammation during acute influenza virus infection by producing IL-10

Jie Sun1, Rajat Madan2, Christopher L Karp2 & Thomas J Braciale1,3

1 Beirne B. Carter Center for Immunology Research, University of Virginia, 409 Lane Road, Charlottesville, Virginia 22908, USA.
2 Division of Molecular Immunology, Cincinnati Children's Hospital Research Foundation, and the University of Cincinnati College of Medicine, 3333 Burnet Avenue, Cincinnati, Ohio 45229, USA.
4 Departments of Microbiology and Pathology, University of Virginia, 409 Lane Road, Charlottesville, Virginia 22908, USA.

Activated antigen-specific T cells produce a variety of effector molecules for clearing infection but also contribute to inflammation and tissue injury. Here we report an anti-inflammatory property of antiviral CD8+ and CD4+ effector T cells (Teff cells) in the infected periphery during acute virus infection. We find that, during acute influenza infection, interleukin-10 (IL-10) is produced in the infected lungs in large amounts—exclusively by infiltrating virus-specific Teff cells, with CD8+ Teff cells contributing a larger fraction of the IL-10 produced. These Teff cells in the periphery simultaneously produce IL-10 and proinflammatory cytokines and express lineage markers characteristic of conventional T helper type 1 or T cytotoxic type 1 cells. Notably, blocking the action of the Teff cell–derived IL-10 results in enhanced pulmonary inflammation and lethal injury. Our results show that antiviral Teff cells exert regulatory functions—that is, they fine-tune the extent of lung inflammation and injury associated with influenza infection by producing an anti-inflammatory cytokine. We discuss the potential implications of these findings for infection with highly pathogenic influenza viruses.

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