摘要
目的:探讨促炎症细胞因子(IL- 6 、IL- 8 、TNF- α) 以及T 细胞亚群在小儿过敏性紫癜发病中的作用。方法:采用双抗体夹心ELISA 法检测30 例急性期、21 例恢复期及28 例健康儿童血清及外周血单个核细胞(PBMC) 培养上清液IL- 6 、IL- 8 及TNF- α水平,以及外周血T 细胞及其亚群的变化。结果:急性期血清及PBMC 上清液IL- 6 、IL-8 、TNF- α水平明显高于恢复期和对照组,且以IL- 8 、TNF- α增高为显著,恢复期上述3 种细胞因子仍高于对照组;外周血CD3 、CD4 、CD8 阳性细胞百分率及淋转率急性期明显低于对照组,至恢复期除CD8 阳性细胞百分率恢复正常外,CD3 、CD4 阳性细胞及淋转率仍低于正常儿;重型病儿血清IL- 8 、TNF- α显著高于轻型病儿,PBMC 诱生的TNF- α水平亦高于较轻型病儿。结论:过敏性紫癜存在多种细胞因子失调,IL- 8 、TNF- α等促炎症细胞因子可能是介导过敏性紫癜血管炎症损伤过程中的重要细胞因子。T 细胞亚群失调及其功能低下是过敏性紫癜重要发病因素之一。
AIM:To explore the effect of proinflammatory cytokines (IL-6, IL-8 and TNF-α) and T lymphocyte subsets on the pathogenesis of anaphylactoid purpura( AP) in children METHODS: Concentration of IL-6, IL-8, TNF-α,in serum and supernatant of peripheral blood mononuclear cells(PBMC) were measured by using enzyme linked immunosorbent assay(ELISA) and T lymphocyte subsets(McAb-A-E method) were detected in 51 cases of AP (acute 30,recovery 21)and 28 cases of healthy children RESULTS:In acute period of AP, levels of IL-6, IL-8, TNF-α in serum and supernatant of PBMC were significantly higher than controls and recovery period ,and in recovery these cytokines were also higher than controls, especially, obvious increase of IL-8 and TNF-α were observed in acute period of AP In acute period , percentage of CD3, CD4, CD8 positive cells and lymphocyte proliferation in peripheral blood were decreased to control level and in recovery the percentage of CD3,CD4 positive cells and lymphocyte proliferation were still lower than healthy children, but CD8 positive cells recovered to normal level Concentratioin of serum IL-8,TNF-α and TNF-α of PBMC superatant in serious AP were higher than that of common AP CONCLUSIONS: There were irregulation of many cytokines in AP, the proinflammatory cytokines IL-8 and TNF-α might be important cytokines in inducing vessel inflammatory lesion of AP The imbalance of T lymphocyte subsets and decrease of its function were important factors in pathogenesis of AP
出处
《中国病理生理杂志》
CAS
CSCD
北大核心
1999年第12期1124-1126,共3页
Chinese Journal of Pathophysiology