期刊
SHOCK
卷 35, 期 3, 页码 252-257出版社
LIPPINCOTT WILLIAMS & WILKINS
DOI: 10.1097/SHK.0b013e3181f489c5
关键词
Differential T-cell signaling; phospho-flow cytometry; burn injury; TCR signaling; CD4(+) regulatory T cells; T-cell activation
资金
- National Institutes of Health [5R01GM035633-22, 2RO1GM57664-09]
Although it is known that injury enhances the regulatory activity of CD4(+) regulatory T cells (Tregs), the cellular and molecular mechanisms responsible for injury-induced Treg activation remain unclear. This study was designed to investigate and compare injury-induced T-cell receptor (TCR) signaling in Tregs, non-Tregs, and CD8(+) T cells. Specifically, we used phospho-flow cytometry to measure the expression and phosphorylation of ZAP-70, protein kinase C theta, nuclear factor of activated T cells, and glycogen synthase kinase 3 beta in FoxP3(+) Tregs versus FoxP3(-) non-Tregs versus CD8(+) T cells. Groups of male C57BL/6J mice underwent burn or sham injury, and lymph nodes and spleens were harvested at early time points-15, 30, 60, 120, and 240 min-to measure TCR signaling. As early as 15 min after burn injury, we observed a significant upregulation and phosphorylation of ZAP-70, protein kinase C theta, nuclear factor of activated T cells, and glycogen synthase kinase 313 in Tregs prepared from injury-site-draining lymph nodes. Burn injury did not activate TCR signaling in Tregs from the spleen or in CD4(+) non-Tregs and CD8(+) T cells. In conclusion, the results of this study demonstrate that burn injury activates TCR signaling in Tregs, but not non-Tregs or CD8(+) T cells. These findings suggest that injury provides an early TCR-activating signal to Tregs and supply new insights into how injury influences the adaptive immune system.
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