Increase of Vδ2 + T Cells That Robustly Produce IL-17A in Advanced Abdominal Aortic Aneurysm Tissues

Abdominal aortic aneurysm (AAA) is a chronic dilation of the aorta with a tendency to enlarge and eventually rupture, which constitutes a major cause of cardiovascular mortality.Although T-cell infiltrates have been observed in AAA, the cellular, phenotypic, and functional characteristics of these tissue-infiltrating T cells are not fully understood. Here, we investigated the proportional changes of T-cell subsets—including CD4 + T cells, CD8 + T cells, and γδ T cells—and their effector functions in AAAs. We found that Vδ2 + T cells were presented at a higher frequency in aortic aneurysmal tissue compared to normal aortic tissue and PBMCs from patients with AAA. In contrast, no differences were observed in the frequencies of CD4 + , CD8 + , and Vδ1 + T cells. Moreover, we observed that the Vδ2 +T cells from AAA tissue displayed immunophenotypes indicative of CCR5 + non-exhausted effector memory cells, with a decreased proportion of CD16 + cells. Finally, we found that these Vδ2 + T cells were the main source of IL-17A in abdominal aortic aneurysmal tissue. In conclusion, our results suggest that increased Vδ2 + T cells that robustly produce IL-17A in aortic aneurysmal tissue may contribute to AAA pathogenesis and progression.

Inverse Relationship between Hepatic Steatosis and Alanine Aminotransferase with Sex Hormone-Binding Globulin in Men

PURPOSE: Sex hormone-binding globulin (SHBG) is a serum glycoprotein produced predominantly in hepatocytes. As such, the synthesis of SHBG could be associated with liver function and metabolic syndrome. Alanine aminotransferase (ALT) levels could reflect hepatocellular injury and insulin resistance; however, the relationship between hepatic steatosis and ALT with SHBG has not been investigated in humans. The objective of this study was to investigate the associations between SHBG and hepatocyte damage among Korean male patients with hepatic steatosis enrolled in a health examination program. MATERIALS AND METHODS: We performed a retrospective cross-sectional study with 922 participants who underwent routine health examinations. A total of 922 men with or without hepatic steatosis were divided into three groups. We analyzed the risk of lower serum SHBG levels with or without elevated serum ALT levels using odds ratios with 95% confidence intervals (CIs). RESULTS: A significantly increased risk of lower serum SHBG level was observed in the group with hepatic steatosis and ALT elevation (95% CI 1.591–4.681). CONCLUSION: In men with hepatic steatosis, we found that elevated serum ALT levels were associated with lower serum SHBG levels. This finding suggests that subjects with both hepatic steatosis and increased ALT should be considered to have low levels of SHBG.