【摘要】 目的　通过测定妊娠高血压综合征 (妊高征 )患者血清封闭抗体对配偶T淋巴细胞的封闭效率来探讨妊高征发病的免疫学机制。　方法　正常孕妇组 82例 ,其中早孕组 16例 ,中孕组32例 ,晚孕组 34例 ;妊高征组 15例 (孕晚期 )。将孕妇血清与配偶T淋巴细胞作用后加入荧光标记的CD3、CD4、CD8单克隆抗体。以流式细胞仪测定所有研究对象的血清封闭抗体对配偶T淋巴细胞分化抗原CD3、CD4、CD8的封闭效率。　结果　正常孕妇组 ,早孕妇女对配偶T淋巴细胞CD3、CD4、CD8的封闭效率分别为 (4.14± 1.0 2、2 .0 2± 0 .2 4、2 .37± 1.0 5 ) % ,高于中孕期 (- 0 .2 9± 0 .13、1.0 3± 0 .2 7和 0 .6 5± 0 .2 3) % (P均 <0 .0 5 ) ;而晚孕期妇女血清对配偶T淋巴细胞CD3、CD4、CD8的封闭效率最低 (- 1.33± 1.4 7、0 .15± 0 .0 1和 - 1.0 4± 0 .37) %。妊高征患者血清对配偶CD3、CD4、CD8的封闭效率 (- 4 .16± 1.2 5、- 2 .13± 0 .4 3和 - 3.38± 1.0 6 ) %明显低于正常晚孕妇女 (P<0 .0 1、0 .0 0 5、0 .0 0 5 )。　结论　 (1)封闭抗体随孕周增加而降低 ,到晚孕期达到最低水平。 (2 )正常妊娠妇女孕早期血清高水平的封闭抗体 ,保证了胚胎早期的正常发育。(3)妊高征患者血清中封闭抗体的减少可能是导致妊高征发病的重更多还原

【Abstract】 Objective To study the association between paternal CD3, CD4 and CD8 antigenecity to their pregnant spouses and the development of pregnancy induced hypertension (PIH). Methods Maternal serum from 15 women with PIH in the third trimester and 82 in normal pregnancies (16 in the first, 32 in the second and 34 in the third trimester) were incubated with paternal T lymphocytes. Monoclonal CD3, CD4 and CD8 fluorescent conjugated antibodies were then added and the percentage of paternal T cell differentiation antigen CD3, CD4 and CD8 were measured by flow cytometry. Results During normal pregnancy, the levels of maternal serum blocking antibodies on paternal CD3, CD4 and CD8 were (4.14±1.02, 2.02 ±0.24, 2.37±1.05)% in first trimester, (-0.29±0.13, 1.03±0.27, 0.65±0.23)% in the second trimester and (-1.33±1.47,0.15±0.01, -1.04± 0.37)% in the third trimester. There were significant difference between them( P<0.05 ).The block ing effects of serum in PIH group on CD3, CD4 and CD8 (-4.16±1.25, -2.13±0.43, -3.38 ± 1.06) % were significantly lower than those of normal third trimester( P<0.01,0.005,0.005 ). Conclusions (1) During normal pregnancy, the maternal serum blocking effect on paternal antigens CD3, CD4 and CD8 decreases with the pregnant progress. (2) High level of blocking antibodies in early normal pregnancy ensures the normal development of the embryo. (3) Impaired maternal production of blocking factors against paternal antigens may be involved in the pathogenesis of PIH.更多还原