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Objective:To investigate the role and the clinical significance of anti-zona pellucidaantibody (AzpAb) and tumor necrosis factor-α(TNF-α),γ-interferon(IFN-γ) and inter-leukin-2 (IL-2) in sera from patients with premature ovarian failure (POF).Methods: The AzpAb in the serum of POF patient was analyzed by means ofELISA. The levels of TNF-α, IL-2 and IFN-γ in the serum were determined by meansof radioimmunoassay (RIA).Results:The level of serum AzpAb in the POF patients was significantly higher thanthat of the normal controls(P<0.001). The levels of TNF-α and IL-2 were significantlyreduced (P<0. 001), and the level of IFN-γ was significantly elevated (P<0.01). Thelevels of above three cytokines in AzpAb positive group were significantly higher thanthose of the negative group in POF patients.Conclusion: This study suggested that AzpAb, TNF-α, IFN-γ and IL-2 might playimportant roles in the pathogenesis of autoimmune POF.

作者:王一峰;韩兰英;欧汝强;杨宁;谢端薇;陈巧儿

来源:生殖医学杂志 2003 年 12卷 z1期

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作者:
王一峰;韩兰英;欧汝强;杨宁;谢端薇;陈巧儿
来源:
生殖医学杂志 2003 年 12卷 z1期
标签:
Premature ovarian failure Anti-zona pellucida antibody Tumornecrosis factor-α Interferon-γ Interleukin-2
Objective:To investigate the role and the clinical significance of anti-zona pellucidaantibody (AzpAb) and tumor necrosis factor-α(TNF-α),γ-interferon(IFN-γ) and inter-leukin-2 (IL-2) in sera from patients with premature ovarian failure (POF).Methods: The AzpAb in the serum of POF patient was analyzed by means ofELISA. The levels of TNF-α, IL-2 and IFN-γ in the serum were determined by meansof radioimmunoassay (RIA).Results:The level of serum AzpAb in the POF patients was significantly higher thanthat of the normal controls(P<0.001). The levels of TNF-α and IL-2 were significantlyreduced (P<0. 001), and the level of IFN-γ was significantly elevated (P<0.01). Thelevels of above three cytokines in AzpAb positive group were significantly higher thanthose of the negative group in POF patients.Conclusion: This study suggested that AzpAb, TNF-α, IFN-γ and IL-2 might playimportant roles in the pathogenesis of autoimmune POF.