原发性胆囊癌患者红细胞变形性及其免疫粘附肿瘤细胞？…

研究、比较原发性胆囊癌（ｐｒｉｍａｒｙ ｇａｌｌｂｌａｄｄｅｒ ｃａｒｃｉｎｏｍａ,ＰＧＣ）患者红细胞变形性及其免疫粘附肿瘤细胞的能力,采用ＢＬ－８８－Ｂ型激光衍激射红细胞变形仪及肿瘤细胞血凝法,检测了２７例原了性胆囊癌患者红细胞变形指数及肿瘤红细胞血凝滴度阳性率与血清中调节因子的变化,并与正常对照组２０例相比较。结果：原发性胆囊癌组红细胞变形指数明显低于正常对照组（Ｐ〈０．００１）,且红细胞免疫     

氯胺酮麻醉对小白鼠红细胞及胸腺免疫功能的影响

本文观察氯胺酮麻醉前后１周小白鼠红细胞免疫粘附功能和红细胞内腺苷脱氨酶的活性。检测结果表明，麻醉后小白鼠红细胞免疫粘附功能及红细胞内ＡＤＡ活力均有明显抑制统计学处理差异非常显著。     

原发性胆囊癌患者红细胞变形性及其免疫粘附肿瘤细胞能力的研究

研究、比较原发性胆囊癌（ｐｒｉｍ ａｒｙ ｇａｌｌｂｌａｄｄｅｒ ｃａｒｃｉｎｏ ｍａ ,ＰＧＣ） 患者红细胞变形性及其免疫粘附肿瘤细胞的能力,采用ＢＬ８８Ｂ 型激光衍射红细胞变形仪及肿瘤细胞血凝法,检测了２７ 例原发性胆囊癌患者红细胞变形指数及肿瘤红细胞血凝滴度阳性率与血清中调节因子的变化,并与正常对照组２０ 例相比较。结果： 原发性胆囊癌组红细胞变形指数明显低于正常对照组（ Ｐ＜ ０ ．００１） ,且红细胞免疫促进因子低于正常对照组,而红细胞免疫抑制因子高于正常对照组（ Ｐ＜ ０ ．０５） 。由此表明,原发性胆囊癌患者的红细胞免疫功能减低与血清中调节因子的变化密切相关。     

体外循环对红细胞免疫调节因子活性的影响

用红细胞免疫调节因子活性测定法，对１３例风心病和１３例先心病病人在体外循环处行心脏手术前后的红细胞免疫粘附促进因子和抑制因子活性进行动态测定。结果显示体外循环术后早期，红细胞免疫粘附促进因子活性降低，抑制因子活性升高；术后２周均恢复至术前状态。本研究初步证实体外循环术后，病人红细胞免疫调节功能紊乱，表现为对红细胞免疫附功能的抑制。     

术后镇痛对红细胞免疫功能的影响

目的 探讨术后镇痛对红细胞免疫功能的影响。方法 择期胆囊切除术患者,ＡＳＡⅠ～Ⅱ级,随机分为镇痛组（以ＶＡＳ≤３分者为试验对象,ｎ＝１５）,与对照组,分别在术前、术后３ｄ、术后７ｄ采静脉血样检测红细胞Ｃ３ｂ受体花环率（ＲＣＲ）、红细胞免疫复合花环率（ＣＩＣＲ）、自然肿瘤红细胞花环率（ＮＴＥＲＴ）、红细胞免疫粘附促进因子（ＲＦＥＲ）及红细胞免疫粘附抑制因子（ＲＦＩＲ）。结果 与对照组相比,镇痛组术前     

红细胞免疫测定在大肠癌中的价值

通过红细胞Ｃ３ｂ受体花环和免疫复合物花环试验，直向肿瘤红细胞花环试验等方法观测５０例大肠癌患者红细胞免疫变化。结果发现，大肠癌患者红细胞免疫功能明显低下，大肠癌患者红细胞免疫功能同肿瘤病理类型，病程，转移途径，血清ＣＥＡ水平有关，大肠癌根治术后患者红细胞免疫功能明显提高，提示红细胞免疫测定可作为大肠癌患者病情，预后判定的辅诊指标。     

重组人促红细胞生成素对尿毒症患者细胞免疫功能和sIL-2R表达的影响

目的观察基因重组人促红细胞生成素（r-HuEPO）对慢性肾衰竭（CRF）患者外周血T-淋巴细胞免疫功能和红细胞免疫功能的影响。方法应用流式细胞仪、双抗体夹心ELISA法和红细胞酵母菌花环实验及红细胞免疫调节因子一步法分别检测观察90例CRF患者经r—HuEPO治疗后,外周血T-淋巴细胞亚群（CD3、CD4和CD4／CD8）、可溶性白介素-2受体（sIL-2R）、红细胞Gb受体花环试验（RNC-C3bRR）、红细胞免疫复合物花环试验（RN2-ICR）、红细胞免疫粘附促进因子（RFAR）和红细胞免疫粘附抑制因子（RFIR）的变化。结果①90例CRF患者外周血清中sIL-2R水平、RBC-ICR和RFIR明显高于正常对照组（P〈0．01）,CD3、CD4、CD4／CD8、RBC-C3bRR和RFAR明显低于正常对照组（P〈0．01）;②r-HuEPO治疗后,RBC—C3bRR、RBC—ICR、RFAR和RFIR均有好转（P〈0．05）,同时sIL-2R、CD3、CD4和CD4／CD8亦有所改善,但无统计学差异（P〉0．05）。结论CRF患者存在明显的细胞免疫功能和红细胞免疫功能低下,rHuEPO治疗对红细胞免疫功能有较好的提升和调节作用,对细胞免疫功能改善不明显。     

星状神经节阻滞对红细胞免疫粘附功能的影响

目的：观察了星状神经节阻滞对红细胞免疫粘附功能的影响。方法：选择适应症患者３３例，进行单侧星状神经节阻滞，每日１次，双侧交替，共７天。并于阻滞前、阻滞后３０分钟及阻滞７天后取外周血测定红细胞－Ｃ３ｂ受体花环率、红细胞－免疫复合物花环率和血清皮质醇的含量。结果：红细胞－Ｃ３ｂ受体花环率在阻滞后３０分钟有明显升高，阻滞７天后仍明显高于阻滞前水平（Ｐ＜０．０５）；红细胞－免疫复合物花环率在阻滞后有下降趋势，但与阻滞前比较无显著性差异（Ｐ＞０．０５）。血清皮质醇在阻滞后３０分钟有非常显著性降低，阻滞７天后仍明显低于阻滞前水平（Ｐ＜０．０１）。红细胞－Ｃ３ｂ受体花环率和血清皮质醇含量的相关分析显示，两者呈反向变化，但不存在直线相关关系。结论：７天连续星状神经节阻滞能提高红细胞免疫粘附功能，可能是通过对下丘脑－垂体－肾上腺轴的影响而发挥调节作用，但并非唯一机制。     

氯胺酮麻醉对小鼠红细胞免疫功能的影响

应用酵母菌花环试验法和红细胞腺苷脱氨酶（简称 ＡＤＡ）活力测定，观察了氯胺酮麻醉对小鼠红细胞免疫功能的影响。检测结果表明，麻醉后红细胞粘附功能及红细胞ＡＤＡ活力均有明显抑制，统计学处理差异有非常显著意义，证明氯胺酮麻醉能够降低红细胞免疫功能。     

胃癌大肠癌病人红细胞免疫功能的变化

观察２５例胃癌和１５例大肠癌病人手术前后一周内红细胞Ｃ３ｂ受体花环试验（ＲＢＣ－Ｃ３ｂ）和红细胞免疫复合物花环率试验，结果显示，胃癌大肠癌病人红细胞Ｃ３ｂ受体免疫粘附功能显著低于正常对照组，部分胃癌病人红细胞免疫复合物花环率显著低于正常人，部分胃癌病人变化不明显，手术和化疗不影响细胞免疫功能，提示红细胞免疫功能缺陷可能是原发或继发，红细胞Ｃ３ｂ受体损坏可能是不可逆的，动态观察红细胞免疫功能有重要的     

Epstein-Barr virus transformation of B lymphocytes from IgA nephropathy patients and first-degree relatives results in increased immunoglobulin synthesis not restricted to IgA.

In order to study B-cell activation patterns independent of T-cell regulation in patients with IgA nephropathy (IgAN), peripheral blood mononuclear cells from 67 patients with IgAN, 15 first-degree relatives of patients with familial disease, and 13 normal controls were transformed with Epstein-Barr virus (EBV). Culture supernatants of these transformed cells were assayed for levels of IgG, IgA, and IgM, and results obtained on the three populations were compared. EBV-transformed cells of IgAN patients, as well as the population of first-degree relatives, secreted significantly elevated levels of all three isotypes as compared with the normal controls. However, in comparing ratios of secreted isotypes, it was determined that more IgA relative to IgG and IgM was synthesized by cells of these two populations as compared with the normal controls. Our results imply that (1) the population of B cells susceptible to EBV activation is increased in IgAN patients; (2) this population of "activatable" B lymphocytes is polyclonal and not restricted to the IgA class; and (3) even though there may be a primary B-cell abnormality in IgAN, an additional defect(s) is probably operative in the pathogenesis, since cells of clinically unaffected relatives behaved in a pattern similar to that of patients.     

Increased immunoglobulin-secreting cells in the blood of patients with active idiopathic IgA nephropathy

Peripheral blood lymphocytes from 33 patients with idiopathic IgA nephropathy (IgAN) and 15 healthy controls were stimulated in vitro by Protein A from Staphylococcus Cowan I; immunoglobulin (Ig) production was measured by a reverse hemolytic plaque assay to evaluate the quantity of cells secreting Ig. In addition, serum Ig levels, circulating IgG, IgA and IgM immune complexes (ICs) and the Fc and C3b receptor mediated phagocytosis of peripheral monocytes were measured. The laboratory findings in different phases of the disease were compared. The mean level of IgA-plaque forming cells (IgA PFC) in IgAN patients with normal renal function was significantly higher (p less than 0.001) than the mean control value. In contrast, they were reduced significantly in those patients who were subjected to periodic hemodialysis (p less than 0.001). Disease activity produced a significant increase in IgG PFC and IgA PFC, high IgG and IgM serum levels, high circulating IgG ICs, and low C3b-mediated phagocytic function of the peripheral macrophages. These findings demonstrate that IgAN is associated with an increased number of IgG and IgA-secreting cells in the peripheral blood of patients during the active phase of the disease and that the concurrent presence of high levels of circulating Ig ICs may be responsible for the gross hematuria, as their deposition in the glomeruli could activate the complement system.     

Effects of interleukin-15 on vascular permeability factor release by peripheral blood mononuclear cells in normal subjects and in patients with minimal-change nephrotic syndrome

The characteristic function of interleukin (IL)-15 appears to be its ability to mimic the stimulatory action of IL-2 on lymphocytes by utilizing part of the IL-2 receptor complex. To gain insight into the immunoregulatory properties of this cytokine in patients with minimal-change nephrotic syndrome (MCNS), we analyzed effects of IL-15 on vascular permeability factor (VPF) release in vitro. Peripheral blood mononuclear cells (PBMC) were isolated from 16 patients with MCNS, 16 patients with IgA nephropathy (IgAN) and 16 healthy controls. Cells were stimulated with concanavalin A (Con A) and the VPF was assessed using the method of Lagrue with minor modifications. PBMC secreted significantly increased amounts of VPF under stimulation with Con A in patients with MCNS and IgAN patients with the nephrotic syndrome as compared with normal controls. Here we have demonstrated, for the first time, that addition of IL-15 to PBMC obtained from nephrotic patients as well as from normal controls increased Con A-induced release of VPF by 250%. This stimulatory effect was found highly significant and was dose-dependent. The effect of IL-15 on the secretion of VPF was specific, since a complete reversion was obtained with a neutralizing antibody to human IL-15. Our findings reveal that IL-15 has the potential to function as an immunoregulatory molecule of PBMC VPF release. In addition, IL-15 had similar effects to IL-2 in terms of its capacity to upregulate VPF release. Taken together, our data emphasize a positive regulatory role for IL-15 in inducing the release of VPF when present at optimal levels. Therefore, IL-15 antagonists may provide a basis for immune intervention in the pathophysiology of VPF.     

Aberrant IgA1 glycosylation is inherited in familial and sporadic IgA nephropathy

IgA nephropathy (IgAN) is a complex trait determined by genetic and environmental factors. Most IgAN patients exhibit a characteristic undergalactosylation of the O-glycans of the IgA1 hinge region, which promotes formation and glomerular deposition of immune complexes. It is not known whether this aberrant glycosylation is the result of an acquired or inherited defect, or whether the presence of aberrant IgA1 glycoforms alone can produce IgAN. A newly validated lectin enzyme-linked immunosorbent assay (ELISA) was used to determine the serum level of galactose-deficient IgA1 (Gd-IgA1) in a cohort of 89 IgAN patients and 266 of their relatives. High Gd-IgA1 levels (> or =95th percentile for controls) were observed in all 5 available patients with familial IgAN, in 21 of 45 (47%) of their at-risk relatives (assuming autosomal dominant inheritance), and in only 1 of 19 (5%) of unrelated individuals who married into the family. This provides evidence that abnormal IgA1 glycosylation is an inherited rather than acquired trait. Similarly, Gd-IgA1 levels were high in 65 of 84 (78%) patients with sporadic IgAN and in 50 of 202 (25%) blood relatives. Heritability of Gd-IgA1 was estimated at 0.54 (P = 0.0001), and segregation analysis suggested the presence of a major dominant gene on a polygenic background. Because most relatives with abnormal IgA1 glycoforms were asymptomatic, additional cofactors must be required for IgAN to develop. The fact that abnormal IgA1 glycosylation clusters in most but not all families suggests that measuring Gd-IgA1 may help distinguish patients with different pathogenic mechanisms of disease.     

Antinuclear autoantibodies in sera of patients with IgA nephropathy

IgA nephropathy (IgAN), assumed to be a chronic immune complex glomerulonephritis, has been sometimes associated with various autoimmune diseases and autoimmune phenomena including autoantibody production. The current study was aimed at thoroughly investigating the frequency of raised autoantibody titers against five common nuclear autoantigens in a large number of patients with IgAN as well as patients with other primary immune complex glomerulopathies and normal controls. The incidence of autoantibodies (greater than 2 SD less than 3 SD of controls) in the IgAN group ranged between 13% in the case of anticardiolipin antibodies, and 19% in the case of antiribonucleoprotein antibodies, yet was not found to be significantly different from the incidence observed in the other control groups. In none of the subjects a titer above 3 SD of the means of controls was found. Our study clearly points to the fact that IgAN, while being an immune-mediated disease, is not a clear-cut autoimmune condition. The finding of autoantibodies in these patients may be merely incidental.     

Blood rheology in IgA nephropathy

Blood rheology was measured in 35 patients with IgA nephropathy (IgAN) and compared with age and sex-matched normal controls. Whole blood viscosity, red blood cell deformability and plasma viscosity were significantly altered in patients with IgAN. A correlation between determinants of blood rheology and clinical indices of IgAN was found. The factor(s) causing the rheological abnormalities was (were) not defined. Increased blood viscosity may cause intraglomerular pressure to rise and filtration to increase and may contribute to the development of mesangial lesions. It is proposed that abnormal blood rheology may be a causal factor in the pathogenesis of IgAN.     

Aberrantly glycosylated serum IgA1 are closely associated with pathologic phenotypes of IgA nephropathy

BACKGROUND: IgA nephropathy (IgAN) is the most common glomerulonephritis with various histologic and clinical phenotypes. The mechanisms underlying the pathogenesis of IgAN remained unclear. But now altered O-glycosylation of serum IgA1 observed in these patients was considered to be a key contributory factor. The aim of the current study is to investigate whether aberrantly glycosylated IgA1 was associated with pathologic phenotypes of IgAN. METHODS: Sera from 107 patients with IgAN recently diagnosed were collected. Fifty patients were with mild mesangial proliferative IgAN, the others were with focal proliferative and sclerosing IgAN. Sera from 22 normal blood donors were used as normal controls. Biotinylated lectins were used in enzyme-linked immunosorbent assay (ELISA) to examine different glycans on IgA1 molecules. The alpha2,6 sialic acid was detected by elderberry bark lectin (SNA), the exposure of terminal galactose (Gal) and N-acetylgalactosamine (GalNAc) were detected by arachis hypogaea [peanut agglutinin (PNA)] and vilsa villosa lectin (VVL), respectively. The serum IgA1 glycans levels corrected by serum IgA1 concentrations were compared between patients and controls. RESULTS: Reduced terminal alpha2,6 sialic acid (1.16 +/- 0.21 vs. 0.98 +/- 0.31) (P= 0.008) and galactosylation (0.30 +/- 0.29 vs. 0.16 +/- 0.19) (P= 0.029) increased exposure of (GalNAc) (0.00 vs. 0.03) (P= 0.024) were demonstrated in serum IgA1 from patients with IgAN as compared with those in controls. More important, the exposures of 2,6 sialic acid and Gal were significantly decreased, especially in patients with focal proliferative and sclerosing IgAN compared with that in patients with mild mesangial proliferative IgAN (0.91 +/- 0.34 vs. 1.05 +/- 0.25) (P= 0.014) (0.108 +/- 0.137 vs. 0.221 +/- 0.219) (P= 0.018). However, no significant difference was found between patients with mild mesangial proliferative IgAN and normal controls (P > 0.05). The exposure of GalNAc of serum IgA1 from patients with focal proliferative and sclerosing IgAN was significantly higher than that of controls (P= 0.017), but had no statistical difference with that of patients with mild mesangial proliferative IgAN. CONCLUSION: The desialylation and degalactosylation of IgA1 in sera of patients with IgAN were closely associated with pathologic phenotypes.     

甘露糖结合蛋白基因多态性与维吾尔族IgA肾病免疫病理类型的关系

目的 探讨甘露糖结合蛋白（MBP）基因多态性与维吾尔族IgA肾病（IgAN）患者免疫病理类型之间的关系。 方法 选择68例经肾活检证实的维吾尔族IgAN患者为对象，对照组为200例维吾尔族健康献血员。采用PCR-RFLP的方法对MBP基因第54位密码子基因多态性进行研究。 结果 （1） 维吾尔族IgAN组与健康对照组MBP-54基因多态性之间差异无统计学意义。（2） 维吾尔族IgAN复合沉积组GAC/GGC 基因型频率显著高于单纯沉积组(44.7% 比 20.0%)；IgAN复合沉积组等位基因GAC的发生频率（0.303）显著高于单纯沉积组（0.133），2组之间的差异有统计学意义（χ2 = 5.461, P < 0.05)。 结论 维吾尔族IgAN 免疫病理多样性受基因背景影响，MBP基因54位点突变型等位基因GAC与维吾尔族IgA肾病免疫复合沉积有关     

人骨肉瘤外周血T淋巴细胞亚群和自然杀伤细胞免疫变化的研究

目的研究人骨肉瘤患者外周血T淋巴细胞亚群和自然杀伤细胞(NK细胞)的变化。方法采用流式细胞术对42例骨肉瘤、41例骨髓炎、34例健康者的外周血CD4 、CD8 、CD4 、CD4 /CD8 、CD3 、CD16 56均显著性低于骨髓炎患者和健康对照组(P<0.01),而CD8 则升高(P<0.05)。骨髓炎患者外周血CD4 、CD4 /CD8 、CD3 较健康人降低,CD8 则升高,但差异均无统计学意义(P>0.05),而CD16 56与健康对照组相比降低(P<0.05)。结论骨肉瘤患者细胞免疫功能明显降低;骨肉瘤患者的免疫抑制远较骨髓炎的强;骨肉瘤患者NK细胞的降低较骨髓炎患者明显多。流式细胞术可作为检测骨肉瘤患者免疫功能的有效方法。