红细胞调控白细胞免疫功能新的自然实验研究体系

目的用血液免疫反应路线图实验体系评估红细胞在白细胞免疫活性中的作用。方法将0·3ml血浆加入0·2ml全血细胞悬液(全血细胞组)或0·2ml白细胞悬液(白细胞组)中,37℃温育1h,用免疫酶联法测定IL-8和IL-12水平,流式细胞仪测定白细胞膜CD4、CD8、CD35和CXCR4表达量。结果全血细胞组IL-8和IL-12水平(分别为5·96±4·26、9·84±2·23ρB·pg-1·ml-1)明显低于白细胞组(分别为15·09±9·86、13·59±3·69ρB·pg-1·ml-1,P<0·05),淋巴细胞CD4、CD35、CXCR4表达量(分别为37·79±12·00、154·66±70·00、34·40±20·45)明显高于白细胞组(分别为18·54±11·32、83·26±35·99、16·69±11·09,P<0.01),粒细胞CD35表达量(603·63±257·64)明显高于白细胞组(384·86±174·16,P<0.01)。成人全血细胞组淋巴细胞和粒细胞CD35和CXCR4表达量明显高于脐血全血细胞组(P<0·05或P<0·01)。结论红细胞是白细胞(包括T淋巴细胞、B淋巴细胞、NK细胞、树突状细胞、粒细胞等)免疫功能的调控者和指导者,脐血红细胞免疫调节功能明显下降;本研究为红细胞免疫调控活性测定提供了新的近似自然的方法。     

抗原激活红细胞和白细胞免疫反应主干道的实验研究

目的测定抗原对红细胞和白细胞免疫反应主干道的作用。方法癌细胞(5×106/ml)和(或)卡介苗(0·1mg)或酵母菌(5×108/ml)加到全血细胞悬液0·2ml(或白细胞0·2ml)和枸橼酸抗凝的新鲜血浆0·3ml(或生理盐水0·3ml)37℃温育1h,采用免疫酶联法检测IL-8水平。分组:①抗原(癌细胞或酵母菌或卡介苗)0·2ml加入全血细胞悬液0·2ml和血浆0·3ml;②生理盐水0·2ml加入全血细胞悬液0·2ml和血浆0·3ml;③抗原0·2ml加入白细胞悬液0·2ml和血浆0·3ml;④生理盐水0·2ml加入白细胞悬液0·2ml和血浆0·3ml。结果癌细胞、卡介苗和酵母菌能激活血液免疫反应,但没有加血浆组中,这些抗原不能激活血液免疫反应,在这些抗原加入全血细胞和血浆组,IL-8激活指数(2·124±0·860)明显高于这些抗原加入白细胞和血浆组的IL-8激活指数(0·390±0·080),P<0·01。结论结果表明在血液免疫反中存在红细胞和白细胞免疫反应主干道路线图,红细胞和补体在血液免疫反应路线图中具有重要作用。     

IgE-mediated anaphylactic reaction to purified and recombinant factor VIII in a patient with severe haemophilia A

We report a 51-year-old patient with severe haemophilia A developing a severe life-threatening anaphylactic reaction to recombinant factor VIII (rFVIII). Anaphylactic reactions are a rare but well-known side effect of FVIII products. The nature of these reactions could not be clarified as previous studies failed to demonstrate a specific IgE response. Here, we could prove a grade 3 anaphlyactic reaction as an IgE-mediated response to rFVIII for the first time by Western blotting.     

P1 blood group antigen expression and epidemic hemolytic uremic syndrome

P1 blood group positivity has been postulated as a host factor which may provide protection against the development of post-enteropathic hemolytic uremic syndrome (HUS). In this study, blood group status in 20 Inuit survivors ofEscherichia coli 0157: H7-associated HUS was compared with age-and sex-matched controls from the same community who had experienced uncomplicated diarrheal illness due to the same pathogen. Of 20 HUS survivors, 6 were P1 antigen positive compared with 8 of the 20 controls (P=0.7). We conclude that P1 antigen positivity was not protective against HUS in this population. Further studies of this condition to clarify the role of host factors in verotoxin-induced endothelial damage are indicated.