In order to study the effect of excessive iodine on immune function of lymphocytes and the role of selenium supplementation with excessive iodine intake,the changes of T lymphocyte number,ratio of subsets,activity of ...In order to study the effect of excessive iodine on immune function of lymphocytes and the role of selenium supplementation with excessive iodine intake,the changes of T lymphocyte number,ratio of subsets,activity of natural killer(NK) cells and lymphocytes proliferation response were investigated.150 female BALB/C mice were randomly divided into 5 groups in terms of their body weight(n=30 in each group),and 10 of each group were taken as one batch for test.Mice in the 5 groups were orally administrated with iodine 0(group Ⅰ),1500(group Ⅱ),3000(group Ⅲ),6000 μg/L(group Ⅳ),iodine 6000 μg/L plus selenium 0.3 mg/L(group Ⅴ) respectively for 30 days.Lymphocyte proliferation response,CD4+/CD8+,Th1/Th2 and the activity of NK cells were meas-ured.CD4+/CD8+ was significantly lower,while lymphocyte proliferation response stronger,and Th1/Th2 and the activity of NK cells significantly higher in group Ⅳ than in group Ⅰ(P<0.01).There was no significant difference in all indexes between group Ⅴ and group Ⅰ(P>0.05).It was suggested that excessive iodine as exogenous chemical materials can induce disorders of T lympho-cyte immune function in mice.0.3 mg/L selenium supplementation can protect mice against toxicity induced by 6000 μg/L iodine.展开更多
基金Project supported by the National Natural Science Foundation of China (No. 20377022, 20237010)the National Basic Research Program (973) of China (No. 2002CB412307).
基金This project was supported by a grant from the National Natural Sciences Foundation of China (No 30230330)
文摘In order to study the effect of excessive iodine on immune function of lymphocytes and the role of selenium supplementation with excessive iodine intake,the changes of T lymphocyte number,ratio of subsets,activity of natural killer(NK) cells and lymphocytes proliferation response were investigated.150 female BALB/C mice were randomly divided into 5 groups in terms of their body weight(n=30 in each group),and 10 of each group were taken as one batch for test.Mice in the 5 groups were orally administrated with iodine 0(group Ⅰ),1500(group Ⅱ),3000(group Ⅲ),6000 μg/L(group Ⅳ),iodine 6000 μg/L plus selenium 0.3 mg/L(group Ⅴ) respectively for 30 days.Lymphocyte proliferation response,CD4+/CD8+,Th1/Th2 and the activity of NK cells were meas-ured.CD4+/CD8+ was significantly lower,while lymphocyte proliferation response stronger,and Th1/Th2 and the activity of NK cells significantly higher in group Ⅳ than in group Ⅰ(P<0.01).There was no significant difference in all indexes between group Ⅴ and group Ⅰ(P>0.05).It was suggested that excessive iodine as exogenous chemical materials can induce disorders of T lympho-cyte immune function in mice.0.3 mg/L selenium supplementation can protect mice against toxicity induced by 6000 μg/L iodine.
文摘同情的 neuronal 区别与 neuroblastoma (NB ) 的有利预后被联系，早童年的最普通的颅外的稳固的肿瘤。区别代理人在 NB 治疗的临床的协议证明了有用，但是因为唯一的治疗不是足够的在病人导致肿瘤消除，使用他们。因此，互补途径例如免疫疗法，被保证。这里，我们证明 NB 房间线和前 vivo 的那区别孤立肿瘤房间响应生理或药理学刺激与增加的 antigenicity 的获得被联系。这是增加了表面专业的表示表明组织亲和性一级建筑群和 ICAM-1 分子并且由细胞毒素的 T 淋巴细胞(CTL ) 和生来的杀手(NK ) 翻译成 NB 房间的增加的敏感到细胞溶解房间。后者是由形式免疫者 conjugates 的区分的房间的提高的能力的 paralleled 并且把 granzyme B 的增加的数量绑在房间表面。 Wedemonstrate ，第一次那不管使用的刺激，在 NB 的区别状态与由细胞毒素的淋巴细胞启用肿瘤房间的更多的有效消除并且在 NB 病人作为一条辅助途径为导致区别的代理人和免疫疗法的联合申请铺平道路的增加的肿瘤 antigenicity 被联系。
基金Supported by Strategic Program of Chinese University of Hong KongDistinguished Young Investigator Fund of the National Natural Science Foundation of China, No. 30029002
文摘瞄准：在氮的氧化物的版本上调查在伤寒上皮细胞和 Peyer 的补丁的淋巴细胞之间的相互作用的效果(没有) 并且响应志贺氏菌属脂肪的多糖(LPS ) 的 IL-6。方法：人的结肠的上皮细胞(Caco-2 ) 是有 Peyer 的补丁从的淋巴细胞的混合 cocultured 野类型(C57 老鼠) 并且可诱导没有 synthase 大美人老鼠，并且与志贺氏菌属 F2a-12 LPS 质问了。版本没有并且 mIL-6 被 Griess 比色测定和连接酶的免疫吸着剂试金(ELISA ) 分别地测量。结果：当 LPS 挑战不在时，不在 Caco-2 上皮细胞的培养基然而并非在 Peyer 的补丁的淋巴细胞被检测，并且 NO 版本在有从也的淋巴细胞的两 cocultures 是进一步起来调整的野类型或 i NOS 大美人老鼠，与一显著地，高水平与 i NOS 猛烈淋巴细胞在 coculture 观察了。在为 24-h 的志贺氏菌属 F2a-12 LPS 挑战以后，没有生产显著地从野类型的老鼠然而并非从 i NOS 猛烈老鼠与 Peyer 的补丁的淋巴细胞在独自一个的 Caco-2 和 coculture 被增加。LPS 被发现从淋巴细胞刺激 mIL-6 的版本，它被 coculture 与 Caco-2 上皮细胞压制。在从 i NOS 猛烈老鼠的淋巴细胞的导致 LPS 的 mIL-6 生产从野类型的老鼠比那显著地大。结论：Peyer 的补丁的淋巴细胞从伤寒维持没有生产的组成的基础水平上皮的房间 Caco-2。从 Peyer 的补丁的淋巴细胞的导致 LPS 的 mIL-6 版本被 cocultured 上皮细胞压制。当没有变化在在淋巴细胞从的没有生产是可检测的时野类型并且在 LPS 前后的 i NOS 猛烈老鼠质问，不从淋巴细胞看起来起一个禁止的作用在上皮响应 LPS 的没有版本和他们的自己的 mIL-6 版本。
