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Shock. 2015 Jun;43(6):589-97. doi: 10.1097/SHK.0000000000000358.

Gamma delta T cells regulate inflammatory cell infiltration of the lung after trauma-hemorrhage.

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*Department of Surgery, The University of Texas Health Science Center, San Antonio; and †US Army Institute of Surgical Research, Fort Sam Houston, Texas.


Trauma-hemorrhage (TH) promotes acute lung injury (ALI) and other pulmonary-related complications in part through an exaggerated inflammatory response. Studies have implicated γδ T cells in the development of inflammatory complications after major injury; however, it is unknown whether γδ T cells play a role in the development of ALI after TH. To study this, C57BL/6 wild-type (WT) and δ TCR mice were subjected to TH or sham treatment. Lung injury was clearly evident at 2 h after TH, as evidenced by increased lung permeability, myeloperoxidase levels, and proinflammatory cytokine/chemokine levels (interleukin-1β [IL-1β], IL-6, IL-10, keratinocyte chemokine, macrophage inflammatory protein 1α, macrophage inflammatory protein 1β, and regulated upon activation normal T-cell expressed, secreted chemokine). Phenotypic analysis of lung cells showed an increase in T-cell numbers after TH. The vast majority of these cells were αβ T cells, irrespective of injury. Although γδ T cells were a small percentage of the total T-cell infiltrate, their numbers did increase after injury. In mice lacking γδ T cells (δ TCR mice), TH-induced T-cell infiltration of the lung was markedly attenuated, whereas infiltration of other inflammatory cells was increased (i.e., monocytes, granulocytes, and myeloid-derived suppressor cells). In conclusion, these findings suggest that γδ T cells regulated the infiltration of the lung with inflammatory cells after injury.

[Indexed for MEDLINE]

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