JNK pathway-associated phosphatase in acute ischemic stroke patients: Its correlation with T helper cells, clinical properties, and recurrence risk.

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.