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

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.

The longitudinal changes of serum JKAP and IL‐17A, and their linkage with anxiety, depression, and cognitive impairment in acute ischemic stroke patients

“…Our recently published study has revealed the dysregulation of JKAP in AIS patients, and this finding is confirmed by the current study 17 ; however, the longitudinal change of JKAP and IL-17A in AIS patients is still unclear. Therefore, the present study further explored this aspect.…”

“…In terms of IL‐17A, it showed an opposite trend to JKAP. The possible reason might be that: (1) IL‐17A is a well‐known proinflammatory cytokine, therefore, changed along with the inflammation during D7; (2) reduced JKAP could boost T helper (Th) 17 cells to secret IL‐17A, then our recently published study also reveals that JKAP negatively relates to IL‐17A in AIS patients 13,14,17 . Therefore, IL‐17A exhibited an opposite trend to JKAP.…”

“…The possible reason might be that: (1) IL‐17A is a well‐known proinflammatory cytokine, therefore, changed along with the inflammation during D7; (2) reduced JKAP could boost T helper (Th) 17 cells to secret IL‐17A, then our recently published study also reveals that JKAP negatively relates to IL‐17A in AIS patients. 13 , 14 , 17 Therefore, IL‐17A exhibited an opposite trend to JKAP. Notably, the clinical role of JKAP is discussed in rheumatic diseases, such as ankylosing spondylitis and rheumatoid arthritis.…”

“… 18 In terms of IL‐17A, it is positively linked with anxiety, depression, and cognitive impairment in AIS patients. 21 Importantly, our recently published study discovers that JKAP is reduced, and negatively related to the National Institutes of Health Stroke Scale (NIHSS) score in AIS patients 17 ; however, the intercorrelation between JKAP and IL‐17A, and their clinical role in estimating psychological health in AIS patients should be further explored.…”

“… 13 , 14 , 15 , 16 Besides, a few studies also report the linkage of JKAP and IL‐17A with mental health in inflammation‐mediated and neurological disease patients. 13 , 17 , 18 , 19 , 20 , 21 For instance, JKAP is reversely linked with cognitive impairment progression in Alzheimer's disease patients. 18 In terms of IL‐17A, it is positively linked with anxiety, depression, and cognitive impairment in AIS patients.…”