γδ T cells protect against LPS-induced lung injury
In: Journal of Leukocyte Biology, Jg. 99 (2015-10-01), S. 373-386
Online
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Zugriff:
γδ T lymphocytes are a unique T cell population with important anti-inflammatory capabilities. Their role in acute lung injury, however, is poorly understood but may provide significant insight into lung-protective mechanisms occurring after injury. In a murine model of lung injury, wild-type C57BL/6 and TCRδ−/− mice were exposed to Escherichia coli LPS, followed by analysis of γδ T cell and macrophage subsets. In the absence of γδ T cells, TCRδ−/− mice developed increased inflammation and alveolar-capillary leak compared with wild-type C57BL/6 mice after LPS exposure that correlated with expansion of distinct macrophage populations. Classically activated M1 macrophages were increased in the lung of TCRδ−/− mice at d 1, 4, and 7 after LPS exposure that peaked at d 4 and persisted at d 7 compared with wild-type animals. In response to LPS, Vγ1 and Vγ7 γδ T cells were expanded in the lung and expressed IL-4. Coculture experiments showed decreased expression of TNF-α by resident alveolar macrophages in the presence of γδ T cells that was reversed in the presence of an anti-IL-4-blocking antibody. Treatment of mice with rIL4 resulted in reduced numbers of M1 macrophages, inflammation, and alveolar-capillary leak. Therefore, one mechanism by which Vγ1 and Vγ7 γδ T cells protect against LPS-induced lung injury is through IL-4 expression, which decreases TNF-α production by resident alveolar macrophages, thus reducing accumulation of M1 macrophages, inflammation, and alveolar-capillary leak.
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γδ T cells protect against LPS-induced lung injury
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Autor/in / Beteiligte Person: | Burnham, Ellen L. ; Wehrmann, Fabian ; Thurman, Joshua M. ; Lavelle, James C. ; Collins, Colm B. ; Tinega, Alex N. ; Simonian, Philip L. |
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Zeitschrift: | Journal of Leukocyte Biology, Jg. 99 (2015-10-01), S. 373-386 |
Veröffentlichung: | Oxford University Press (OUP), 2015 |
Medientyp: | unknown |
ISSN: | 1938-3673 (print) ; 0741-5400 (print) |
DOI: | 10.1189/jlb.4a0115-017rr |
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