%0 Journal Article %T Deficiency of ¦Ã¦ÄT cells protects against abdominal aortic aneurysms by regulating phosphoinositide 3-kinase/AKT signaling - Journal of Vascular Surgery %A Bin You %A Congcong Zhang %A Guang Li %A Jie Du %A Ping Li %A Shuai Zhang %A Xiaoyu Kan %A Yulin Li %J Journal of Vascular Surgery Home Page %D 2018 %R https://doi.org/10.1016/j.jvs.2016.03.474 %X It is known that T lymphocytes are activated in human abdominal aortic aneurysms (AAAs). ¦Ã¦ÄT cells, as a subset of T cells, play a role in many inflammation-related diseases. However, whether ¦Ã¦ÄT cells participate in the formation of AAA remains unknown. In this study, we explored the role of ¦Ã¦ÄT cells in AAA lesions. Using the porcine pancreatic elastase-induced AAA model, we found that knock out of ¦Ã¦ÄT cells significantly attenuated AAA formation. To elucidate how ¦Ã¦ÄT cells contribute to AAA, microarray analysis was performed, which found that the phosphoinositide 3-kinase/AKT signaling pathway was activated in elastase-perfused ¦Ã¦ÄT knockout (¦Ã¦ÄT KO) mice. By studying differentially expressed genes involved in phosphoinositide 3-kinase signaling, we found that proliferation-related genes (Sos1, Mtor, Myc) were upregulated whereas apoptosis-related genes (Pten, Bcl1, Bad) were downregulated in elastase-perfused ¦Ã¦ÄT KO mice. Furthermore, histopathologic analysis showed increased PCNA+ and decreased TUNEL+ cells in elastase-perfused ¦Ã¦ÄT KO mice compared with wild-type mice. In addition, inflammatory cytokines including interleukin-1¦Â, Mcp-1, and tumor necrosis factor-¦Á were downregulated in the aneurysm tissues of elastase-perfused ¦Ã¦ÄT KO mice. These data reveal a pathogenic role of ¦Ã¦ÄT cells in the experimental AAA model, likely through mechanisms regulating cell proliferation and mediating inflammatory response. Thus, targeting of ¦Ã¦ÄT cells may offer a potential therapeutic method for aortic aneurysms. Abdominal aortic aneurysm (AAA) is now considered to be an inflammatory disease. Despite numerous advances in therapeutic strategies, the mortality rate still remains high because of the progressive expansion and sudden rupture. Increasing evidence has demonstrated an important role of inflammatory response in mouse models of AAA. It has been proved that AAA formation is accompanied by infiltration of T lymphocytes. In this study, we proved the functions of ¦Ã¦ÄT cells regulating inflammation, cell proliferation, and apoptosis. Taken together, our findings suggested that the ¦Ã¦ÄT cell is crucial for the development of AAA and may offer a potential therapeutic target for aortic aneurysm. %U https://www.jvascsurg.org/article/S0741-5214(16)31854-7/fulltext