Jie Ying, Pan Zhi-qiang, Chen Yu, Zhang Wen-hua, Xu Liang, Wu Yu-ying, Peng Hong
Beijing Institute of Ophthalmology, Beijing Tongren Eye Centre, Beijing Tongren Hospital, Capital University of Medical Sciences, Beijing 100730, China.
Zhonghua Yan Ke Za Zhi. 2005 Feb;41(2):150-5.
To determine the mechanism of staphylococcal enterotoxin B (SEB) induced immune tolerance in the treatment of high-risk corneal transplantation in the rat.
Fisher 344 rats were used as donors and Lewis rats were used as recipients. Corneal neovascularization was induced by sutures. The rats were divided randomly into five groups in a masked fashion. In the 4 SEB-treated groups, 0.2 ml SEB were intraperitoneally injected before the keratoplasty at concentrations of 25 microg/kg, 50 microg/kg, 75 microg/kg and 100 microg/kg, respectively. The control group received a saline buffer injection intraperitoneally. All allografts were observed and scored for 30 days. Meanwhile, the infiltration of lymphocytes in the allografts, the percentage of lymphocyte subpopulations in the immune organs, the proliferation ability of the lymphocytes and the cytokines in the serum were measured.
The SEB at the concentration of 25 microg/kg did not prolong the survival time of the allografts as compared to the control group. With the increase of the concentration of SEB, the survival time in the other three SEB-treated groups were prolonged significantly and the 75 microg/kg group showed the best results. The infiltration of the lymphocytes in the allografts and the percentages of CD4+ and CD8+ lymphocytes in the immune organs in the SEB treated groups were reduced. The proliferation ability of the lymphocytes in SEB treated groups was decreased; the concentration of IL-2 was lower while the concentration of IL-10 was higher in the serum in the SEB treated groups.
SEB at an optimal concentration is effective in inhibiting immune rejection in high-risk corneal transplantation. The mechanism of SEB induced immune tolerance is related to the reduction of the number and the immune tolerance status of the lymphocytes.
确定葡萄球菌肠毒素B（SEB）诱导免疫耐受在大鼠高危角膜移植治疗中的机制。
以Fisher 344大鼠为供体，Lewis大鼠为受体。通过缝线诱导角膜新生血管形成。将大鼠以盲法随机分为五组。在4个SEB治疗组中，分别在角膜移植术前腹腔注射0.2 ml浓度为25μg/kg、50μg/kg、75μg/kg和100μg/kg的SEB。对照组腹腔注射生理盐水缓冲液。对所有同种异体移植物进行30天的观察和评分。同时，检测同种异体移植物中淋巴细胞的浸润情况、免疫器官中淋巴细胞亚群的百分比、淋巴细胞增殖能力以及血清中的细胞因子。
与对照组相比，25μg/kg浓度的SEB未延长同种异体移植物的存活时间。随着SEB浓度的增加，其他三个SEB治疗组的存活时间显著延长，75μg/kg组效果最佳。SEB治疗组同种异体移植物中淋巴细胞的浸润以及免疫器官中CD4+和CD8+淋巴细胞的百分比降低。SEB治疗组淋巴细胞的增殖能力下降；SEB治疗组血清中IL-2浓度较低而IL-10浓度较高。
最佳浓度的SEB可有效抑制高危角膜移植中的免疫排斥反应。SEB诱导免疫耐受的机制与淋巴细胞数量的减少及其免疫耐受状态有关。
