摘要
Background Inhibition of the key costimulatory signals results in T cell anergy, indicating the alloantigen-specific immunologic unresponsiveness. In this study, the effect of blockage of costimulatory signal CD86 on murine abortion-prone model was studied. Methods Thirty CBA/J female mice cohabitated with DBA/2 male or BALB/c male mice were investigated. CBNJ xDBN2 matings were used as the abortion-prone model, and CBA/J × BALB/c matings were used as the normal pregnant model. The abortion-prone models were divided into experimental and control groups, and the normal pregnant models were set as a normal group （10 mice in each group）. The mice in the experimental group were treated with anti-mouse CD86 monoclonal antibody （mAb） （100 μg） on day 4.5 of gestation, while the controls received irrelevant-isotype matched rat IgG2b. As for the normal group, nothing was given to the mice. The mice were killed on day 13.5 of gestation, embryo resorption rate and the expression of transforming growth factor β1 （TGF-β1）, plasminogen activator inhibitor 1 （PAI-1）, and matrix metalloproteinase 9 （MMP-9） were detected. Then the data were analyzed by Chi-square test and Fisher＇s exact test. Results The embryo resorption rate in the experimental （8.2%） and normal groups （7.7%） was significantly lower than that of the control （23.5%, P〈0.05）. No significant difference was detected between the experimental and normal groups （P〉0.05）. The positive expression rates of TGF-β1 and PAl-1 proteins in the experimental and normal groups were significantly higher than those in the control group （P〈0.05）. The positive expression rate of MMP-9 protein in the experimental and normal groups was significantly lower than that in the control group （P〈0.05）. No significant difference in the positive expression rates of the three proteins was detected between the experimental and normal groups （P〉0.05）. Conclusions Blockage of costimulatory signal CD86 at early pregnancy can treat
Background Inhibition of the key costimulatory signals results in T cell anergy, indicating the alloantigen-specific immunologic unresponsiveness. In this study, the effect of blockage of costimulatory signal CD86 on murine abortion-prone model was studied. Methods Thirty CBA/J female mice cohabitated with DBA/2 male or BALB/c male mice were investigated. CBNJ xDBN2 matings were used as the abortion-prone model, and CBA/J × BALB/c matings were used as the normal pregnant model. The abortion-prone models were divided into experimental and control groups, and the normal pregnant models were set as a normal group （10 mice in each group）. The mice in the experimental group were treated with anti-mouse CD86 monoclonal antibody （mAb） （100 μg） on day 4.5 of gestation, while the controls received irrelevant-isotype matched rat IgG2b. As for the normal group, nothing was given to the mice. The mice were killed on day 13.5 of gestation, embryo resorption rate and the expression of transforming growth factor β1 （TGF-β1）, plasminogen activator inhibitor 1 （PAI-1）, and matrix metalloproteinase 9 （MMP-9） were detected. Then the data were analyzed by Chi-square test and Fisher＇s exact test. Results The embryo resorption rate in the experimental （8.2%） and normal groups （7.7%） was significantly lower than that of the control （23.5%, P〈0.05）. No significant difference was detected between the experimental and normal groups （P〉0.05）. The positive expression rates of TGF-β1 and PAl-1 proteins in the experimental and normal groups were significantly higher than those in the control group （P〈0.05）. The positive expression rate of MMP-9 protein in the experimental and normal groups was significantly lower than that in the control group （P〈0.05）. No significant difference in the positive expression rates of the three proteins was detected between the experimental and normal groups （P〉0.05）. Conclusions Blockage of costimulatory signal CD86 at early pregnancy can treat
基金
This work was supported by the grants from the Technology Department of National Population and Family Planning Commission of China (No. 2005 C1-41).
