J Clin Lab Anal. 2022 Jul 8:e24535. doi: 10.1002/jcla.24535. Online ahead of print.
ABSTRACT
OBJECTIVE: JKAP modifies T-cell immune response and inflammation, also involves in cardia-cerebrovascular disease etiology. This study intended to explore JKAP’s relation with T-helper 1 (Th1), T-helper 17 (Th17) cell levels, clinical properties, and recurrence-free survival (RFS) in acute ischemic stroke (AIS) patients.
METHODS: A total of 155 AIS patients were analyzed. Serum JKAP, interferon-gamma (IFN-γ), and interleukin-17A (IL-17A) were detected by ELISA; then blood Th1 and Th17 cells were quantified by flow cytometry. Besides, 30 healthy subjects were enrolled as controls to detect JKAP, Th1, and Th17 cells.
RESULTS: JKAP level was lower (p < 0.001), Th1 cells were not differed (p = 0.068), but Th17 cells were elevated in AIS patients versus controls (p < 0.001). Meanwhile, JKAP was negatively correlated with Th1 cells (p = 0.038), Th17 cells (P<0.001), IFN-γ (p = 0.002), and IL-17A (p < 0.001) in AIS patients. JKAP was negatively associated with the National Institutes of Health Stroke Scale (NIHSS) score (p < 0.001), but Th17 cells (p = 0.001), IFN-γ (p = 0.035), and IL-17A (p = 0.008) levels were positively associated with NIHSS score. Additionally, accumulating RFS was numerically longer in patients with JKAP Quantile (Q) 4 than patients with JKAP Q1-Q3 (p = 0.068), and numerically better in patients with JKAP Q3-Q4 than patients with JKAP Q1-Q2 (p = 0.069), but without statistical significance.
CONCLUSION: JKAP correlates with lower Th1 and Th17 cell percentages as well as milder disease severity.
PMID:35808912 | DOI:10.1002/jcla.24535
