脑出血后的病理改变与T淋巴细胞反应

目的:探讨脑出血血肿周围局部病理改变及细胞免疫机制。方法:用免疫组化方法及组织HE染色法观察20只大鼠尾壳核脑出血24 h,3天、7天血肿周围区域的组织病变及CD3 、CD8 T淋巴细胞的分布形式和表达时程。结果:①在脑出血后24 h血肿周围即可见明显血管源性水肿,大量炎性细胞浸润,以中性粒细胞为主,少量散在淋巴细胞、小胶质细胞、星形细胞、少突胶质细胞弥漫浸润;出血3天、7天以淋巴细胞、巨噬细胞浸润为主,小胶质细胞、星形细胞、少突胶质细胞增生明显,双侧半球皮层下和血管周围出现小胶质细胞结节;②出血灶周围CD3 和CD8 T淋巴细胞浸润在出血后24 h已可见,出血后3天组和出血后7天组,CD3 和CD8 阳性细胞数明显高于出血后24 h组。结论:①脑出血期以中性粒细胞反应为主,以后以淋巴细胞反应为主,胶质细胞反应在出血后24 h已发生,持续一周以上;②CD3 、CD8 阳性细胞的出现提示它们参与了出血后脑损伤的病理过程,在出血7天内, CD3 和CD8-阳性细胞反应呈增强趋势。     

冠心病患者治疗前后血清SOD、ET及T淋巴细胞亚群水平

目的:探讨了冠心病患者治疗前后血清SOD、ET及T淋巴细胞亚群水平。方法:分别应用放免法和单克隆抗体法对42例冠心病患者进行了血清SOD、ET及T淋巴细胞亚群水平检测,并与35名正常健康人作比较。结果:冠心病患者在治疗前血清ET水平显著地高于正常人组(P<0.01),而SOD和CD4/CD8比值明显地低于正常人组(P<0.01),经治疗后一个月则与正常人组比较差异无显著性(P>0.05)。结论:检测冠心病患者血清SOD、ET及T淋巴细胞亚群水平对判断病情及其预后均具有一定的临床实用价值。     

A monoclonal antibody (RH1-38) which inhibits multiple systems of cell-mediated cytotoxicity--I. Identification of a novel epitope on a killer cell surface bimolecular complex important in the cytotoxic response

This paper presents the initial characterization of a mouse monoclonal antibody (RH1-38) which blocks, in the absence of complement, three different systems of cell-mediated cytotoxicity. This monoclonal antibody markedly inhibits cytotoxicity mediated by human natural killer cells, a monocyte-like cell [phorbol myristate acetate (PMA) stimulated HL-60], and cytotoxic T-lymphocytes generated in a mixed leukocyte reaction. RH1-38 is not nonspecifically toxic to cells since antibody-dependent cellular cytotoxicity was not inhibited and viability as assessed by trypan blue exclusion was not affected. Inhibition is specific since control hybridoma culture supernatants, parent (NS-1) ascites supernatant, monoclonal anti-HLA and normal mouse IgG were not significantly inhibitory. In the NK system, the inhibitory effect appears to be due to binding of monoclonal antibody to effector cell surface since exposure of targets to antibody followed by washing yielded no inhibition of killing. Inhibition requires the antigen-binding portion of the antibody molecule and thus appears to be related to steric hindrance of an effector cell surface molecule which is important in the expression of cell-mediated cytotoxicity. Immunoprecipitation of surface-radioiodinated membranes from PMA-stimulated HL-60 cells and analysis on sodium dodecyl sulfate-polyacrylamide gels revealed a bimolecular complex (195,000 and 125,000 daltons) without significant change under reducing conditions. Control immunoprecipitates yielded no peaks of activity. This monoclonal antibody should serve as a useful probe of the function and biochemistry of a killer cell surface antigen important in the expression of cell-mediated cytotoxicity. Since RH1-38 inhibits cytotoxicity mediated by at least three apparently unrelated effector cells, the relevant antigen may be part of a common mechanistic step. As the companion paper demonstrates, this monoclonal antibody does not affect the conjugation step, but appears to block a late step in the NK cytolytic mechanism. Thus, RH1-38 recognizes either an epitope district from previously-described anti-LFA-1 antibodies or alternatively recognizes a distinct functional killer cell surface molecule.     

The influence of radiation therapy on T-lymphocyte subpopulations defined by monoclonal antibodies

We studied the influence of radiation therapy on lymphocyte subpopulations in 17 patients undergoing adjuvant radiation therapy for primary breast cancer, and eight patients receiving brachytherapy and external beam irradiation for primary cancer of the uterus. Radiation therapy reduced B- and T-lymphocytes in proportion to the total lymphocyte population so that their percentages remained unchanged. Determination of helper and suppressor T-lymphocytes before, during and 6 months after completion of radiotherapy revealed that in both groups of patients suppressor T-lymphocytes were more resistant to and recovered faster after radiotherapy. This resulted in a decline of the "immunoregulatory balance" (helper/suppressor ratio). Although this ratio had been higher in both groups of patients than in healthy age- and sex-matched controls before therapy, it became normal and subnormal during and after radiotherapy. The clinical significance of the differential influence of radiotherapy on T-lymphocyte subpopulations remains to be determined.     

五种免疫相关性心血管疾病的免疫学研究

对扩张型心肌病、风湿性心脏病，原发性高血压，冠心病及肥厚型心肌病进行外周血清可溶性白细胞介素２受体，Ｔ淋巴细胞亚群及自然杀伤细胞活性的检测，并与健康对照组比较，结果显示：ＤＣＭ组，ＲＨＤ组及ＥＨＴ组的ｓＩＬ－２Ｒ明显高于ＮＣ组，而ＤＣＭ、ＲＨＤ风湿活动组的ＮＫ活性低于ＮＣ组，ＥＨＴ组ＮＫ活性高于ＮＣ组。     

烧伤后血清触珠蛋白对T淋巴细胞功能的影响

采用亲和层析法从烧伤血清纯化触珠蛋白（Ｈａｐｔｏｇｌｏｂｉｎ，ＨＰ）后，体外观察了纯化ＨＰ对正常小鼠胸腺细胞在ｃｏｎＡ刺激下增殖与ＩＬ－２产生及对ＩＬ－２诱导的ＩＬ－２依赖细胞株（ＣＴＬＬ－２）增殖的影响。结果表明，纯化ＨＰ在相当于烧伤血清ＨＰ浓度时，对小鼠胸腺细胞增殖、ＩＬ－２产生及ＣＴＬＬ－２增殖具有非常明显的抑制作用；但在相当于正常血清ＨＰ浓度时纯化ＨＰ则无抑制作用。提示烧伤血清高浓度的ＨＰ可能是烧伤后Ｔ淋巴细胞免疫功能低下的一个重要原因。     

慢性扁桃体炎病儿细胞免疫功能的变化

1目的　探讨慢性扁桃体炎病儿细胞免疫功能的变化及临床意义。2方法　采用碱性磷酸酶抗碱性磷酸酶法及红细胞酵母菌花环法 ,检测了 40例慢性扁桃体炎病儿及 30例健康儿童红细胞 C3b受体花环率 (E- C3bRR )、红细胞免疫复合物花环率 (E- ICR)、T淋巴细胞亚群和可溶性白细胞介素 2受体 (s IL - 2 R)的变化。3结果慢性扁桃体炎病儿外周血 T淋巴细胞亚群 CD4阳性细胞及 CD4/ CD8比值较对照组降低 (t=2 .10 ,3.70 ,P <0 .0 1,0 .0 5 ) ,CD8阳性细胞较对照组升高 (t=6 .83,P<0 .0 1) ;E- C3b RR,E- ICR较对照组降低 (t=10 .47,3.35 ,P<0 .0 1) ;血清中 s IL- 2 R水平较对照组升高 (t=9.11,P<0 .0 1) ;CD4/ CD8比值与 s IL- 2 R水平呈显著负相关 (r=- 0 .8436 ,P<0 .0 1)。4结论　慢性扁桃体炎病儿细胞免疫功能低下且紊乱。     

尿毒症患者T淋巴细胞及其亚群改变的观察

目的了解尿毒症患者Ｔ淋巴细胞及其亚群的改变,探讨其临床意义。方法从外周血分离淋巴细胞,用抗人Ｔ淋巴细胞及其亚群的单克隆抗体直接测定。结果用ｔ检验及直线回归分析。结果尿毒症患者与正常组比较,Ｔ淋巴细胞总数（ＣＤ３）、辅助Ｔ淋巴细胞（ＣＤ４）数降低（Ｐ＞０．０５）,抑制Ｔ淋巴细胞（ＣＤ８）数明显升高（Ｐ＜０．０１）,ＣＤ４／ＣＤ８明显降低（Ｐ＜０．０５）;肾小球滤过率（ＧＦＲ）与ＣＤ８呈显著负相关（ｒ＝－０．８４８）,与ＣＤ４／ＣＤ８呈显著正相关（ｒ＝＋０．７８２）。在慢性肾炎与非慢性肾炎所引起的尿毒症中,Ｔ淋巴细胞及其亚群的改变没有差异。结论在尿毒症患者,ＣＤ８和ＣＤ４／ＣＤ８的改变可以作为免疫功能低下的指标     

增免灵对活动性肺结核患者的疗效及外周血T淋巴细胞亚群的影响

目的　比较常规疗法伍用增免灵与单用常规疗法对活动性肺结核的疗效及外周血Ｔ 淋巴细胞亚群的影响。方法　抽取常规化疗组（６１ 例）、常规化疗加增免灵组（７２ 例） 及健康对照组（３５ 例） 患者外周血,用ＡＰＡＡＰ法测定外周血淋巴细胞亚群。结果　活动性肺结核患者外周血ＣＤ＋３ 及ＣＤ＋４ 百分率及ＣＤ＋４ ／ＣＤ＋８ 比值显著低于健康对照组（ Ｐ＜ ０．０５） ,ＣＤ＋８ 高于健康对照组。结论　短程化疗伍用增免灵可显著改善活动性肺结核的疗效及细胞免疫状况。     

子宫内膜异位症患者免疫功能的变化

目的　为了探讨子宫内膜异位症发病的免疫机制。方法　采用间接免疫荧光法对子宫内膜异位症患者外周血中的 Ｔ细胞亚群、 Ｂ 细胞, Ｎ Ｋ 细胞及 Ｉ Ｌ－ ２ Ｒ＋ 细胞进行检测,并采用酶联免疫双抗体夹心法对子宫内膜异位症患者外周血及腹腔液中的 Ｔ Ｎ Ｆ－ α浓度进行了检测。结果　子宫内膜异位症患者外周血中 Ｔ 细胞亚群失衡、 Ｂ 细胞增多,外周血及腹腔液中的 Ｔ Ｎ Ｆ－ α浓度显著升高。结论　外周血中 Ｔ 细胞亚群失衡、 Ｂ 细胞增多,腹腔液中 Ｔ Ｎ Ｆα浓度升高可能与子宫内膜异位症的发生,发展密切相关。