期刊
PLOS ONE
卷 7, 期 2, 页码 -出版社
PUBLIC LIBRARY SCIENCE
DOI: 10.1371/journal.pone.0032371
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资金
- Centre of Respiratory Infections (CRI)
- MRC & Asthma UK Centre in Allergic Mechanisms of Asthma
- European Commission [UU-ER/2010/010744]
- Wellcome Trust [087805/Z/08/Z]
- MRC [G0800311]
- MRC [G0800311, MC_U117565642] Funding Source: UKRI
- Asthma UK [S06/001] Funding Source: researchfish
- Medical Research Council [G1000758B, G0800311, G1000758, MC_U117565642] Funding Source: researchfish
- National Institute for Health Research [NF-SI-0508-10212] Funding Source: researchfish
Interleukin (IL-) 10 is a pleiotropic cytokine with broad immunosuppressive functions, particularly at mucosal sites such as the intestine and lung. Here we demonstrate that infection of BALB/c mice with respiratory syncytial virus (RSV) induced IL-10 production by CD4(+) and CD8(+) T cells in the airways at later time points (e. g. day 8); a proportion of these cells also co-produced IFN-gamma. Furthermore, RSV infection of IL-10(-/-) mice resulted in more severe disease with enhanced weight loss, delayed recovery and greater cell infiltration of the respiratory tract without affecting viral load. In addition, IL-10(-/-) mice had a pronounced airway neutrophilia and heightened levels of pro-inflammatory cytokines and chemokines in the bronchoalveolar lavage fluid. Notably, the proportion of lung T cells producing IFN-gamma was enhanced, suggesting that IL-10 may act in an autocrine manner to dampen effector T cell responses. Similar findings were made in mice treated with antiIL-10R antibody and infected with RSV. Therefore, IL-10 inhibits disease and inflammation in mice infected with RSV, especially during recovery from infection.
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