The TH22‐mediated IL‐22 deficiency associated with premature ovarian insufficiency

Abstract

AbstractResearch questionIs deficiency of IL‐22 associated with premature ovarian insufficiency (POI)?DesignLevels of IL‐22 and IL‐22BP, IL‐22‐producing T cells, and IL22RA1/IL10R2 expression were measured and compared among 29 patients with POI, 42 with precursor stage of POI (pre‐POI) and 46 control women. Correlation of serum IL‐22 and IL‐22+CD4+T subsets with ovarian reserve markers were further analyzed.ResultsIL‐22 levels in serum significantly differed among control women and patients with pre‐POI and POI, with the lowest concentrations in POI group (p = .019). Significant reduction of peripheral CD4+IL‐22+T cells was observed in patients with POI (p = .010), which mainly contributed by decrease of CD4+IL‐22+IL‐17− TH22 cells (p = .012) but not TH17 cells (p = .125). Levels of serum IL‐22 and IL‐22‐producing CD4+T subsets were significantly correlated with ovarian reserve markers, including AMH, bilateral AFC, follicle‐stimulating hormone (FSH), and E2 (p < .05). The specific receptor IL22RA1 expression was marginally reduced in granulosa cells from patients with pre‐POI (p = .051). No difference of IL‐22BP was observed either in serum (p = .216) or follicular fluid (p = .856) among groups.ConclusionsOur study first demonstrated the significant association between TH22‐mediated IL‐22 deficiency and ovarian insufficiency, which provide new insights into the autoimmune disturbance and opens new avenues for exogenous IL‐22 administration as potential intervention of POI.