急性白血病患者的血清红细胞免疫抑制活性

急性白血病患者存在红细胞免疫功能的缺陷业已为实验所证实。这种免疫低下被认为与细胞膜上C_3b受体的数目及活性的降低有关。但有关急性白血病患者血清红细胞免疫抑制活性的研究很少。本文对33名急性白血病患者的血清红细胞免疫抑制活性进行了检测,同时对其与红细胞免疫粘附作用的相关关系进行了探讨。     

老年糖尿病患者红细胞免疫功能的研究

本文对34例老年糖尿病患者红细胞免疫粘附功能及其调节因子活性进行了测定。结果显示,老年糖尿病患者红细胞C_3b受体花环率较正常对照组明显降低(P<0.01),免疫粘附抑制率明显升高(P<0.01),红细胞C_3b受体花环率降低和免疫粘附抑制率升高与高血糖、高血脂均呈负相关。提示老年糖尿病患者红细胞免疫功能低下,红细胞免疫粘附抑制因子降低,高血糖、高血脂可能是导致红细胞免疫功能低下的重要因素。     

脾切除对晚期血吸虫病患者细胞免疫调节失常的影响

对30例巨脾型和19例已切脾的晚期血吸虫病(晚血)患者及 41例对照人群进行外周血 NK细胞活性、红细胞C_(3b)受体花环率、中性粒细胞吞噬功能和淋巴细胞转化试验测定以检测晚血患者的细胞免疫功能变化及脾切除对其影响。结果显示,晚血巨脾型患者上述免疫功能均明显低于对照人群,切脾患者 NK细胞活性、红细胞C_(3b)受体花环率明显高于巨脾组。晚血患者中性粒细胞吞噬指数及淋巴细胞转化功能已呈抑制,但切脾组与巨脾组之间无明显差异。表明脾切除不仅能降低门脉高压,同时也有可能改善患者的细胞免疫调节功能,增加患者抵抗力。     

急慢性肝炎患者红细胞免疫粘附功能变化

目的探讨各型肝炎时红细胞免疫粘附功能的变化。方法用红细胞 C_3b 受体花环及免疫复合物花环法测定了42例急慢性肝炎患者活动期及恢复期的红细胞免疫粘附功能.同时测定了血浆免疫复合物水平变化。结果 B 型肝炎活动期红细胞 C_3b 受体花环形成率明显下降,分别为:急性肝炎13.54%±5.23%,急性重症肝炎7.61%±4.12%,慢性肝炎13.96%±5.01%,均低于正常(18.12%±3.91%)。恢复期则逐渐回升。红细胞免疫复合物花环及血浆免疫复合物均高于正常。结论急慢性肝炎时红细胞免疫粘附功能下降,其下降幅度与病情程度呈正比。     

囊尾蚴病患者红细胞免疫粘附功能的研究

目的 :探讨囊尾蚴病患者红细胞免疫粘附功能 ( RCIA)变化及其机制。方法 :用酵母菌标记技术检测囊尾蚴病患者红细胞表面 C3b受体活性及 RCIA调节因子活性 ;用琼脂单扩散法测血清补体 C3含量 ,用聚乙二醇 -紫外分光法测血清 CIC含量。结果 :囊尾蚴病患者红细胞膜 C3b受体花环率及血清 RCIA增强因子活性明显低于正常对照组 ,而红细胞膜 IC花环率 ,血清中免疫粘附抑制因子活性及血清中 CIC含量较正常对照组明显升高。结论 :囊尾蚴病患者红细胞膜 C3b受体活性受损 ,清除 CIC能力下降。     

偏头痛患者红细胞免疫功能的初步研究

本文测定了45例偏头痛患者及相应对照组的红细胞膜受体含量变化。结果表明:偏头痛发作期病人的红细胞C_(3b)受体花环率明显低于对照组,而免疫复合物受体花环率明显高于对照组。两种受体花环率间具有显著负相关性。提示红细胞免疫粘附功能异常参与了偏头痛症状的发作。     

动脉粥样硬化性脑梗死患者红细胞的免疫功能改变

探讨动脉粥样硬化性脑梗死患者红细胞免疫粘附功能变化的特点.观察了86例动脉粥样硬化性脑梗死患者和63例正常对照者的红细胞免疫功能4项指标红细胞C3b受体花环率、红细胞免疫复合物花环率、血清中红细胞免疫粘附增强因子及红细胞免疫粘附抑制因子.动脉粥样硬化性脑梗死患者红细胞免疫功能变化的特点是红细胞C3b受体花环率降低,红细胞免疫复合物花环率升高,同时伴有血清中红细胞免疫粘附增强因子活性降低及红细胞免疫粘附抑制因子活性增强,红细胞免疫粘附功能低下.本研究提示脑梗死患者红细胞免疫功能下降,为探讨动脉粥样硬化性脑梗死的发病与防治途径提供了依据.     

动脉粥样硬化性脑梗死患者红细胞的免疫功能改变

探讨动脉粥样硬化性脑梗死患者红细胞免疫粘附功能变化的特点。观察了86例动脉粥样硬化性脑梗死患者和63例正常对照者的红细胞免疫功能4项指标：红细胞G3b受体花环率、红细胞免疫复合物花环率、血清中红细胞免疫粘附增强因子及红细胞免疫粘附抑制因子。动脉粥样硬化性脑梗死患者红细胞免疫功能变化的特点是红细胞G3b受体花环率降低，红细胞免疫复合物花环率升高，同时伴有血清中红细胞免疫粘附增强因子活性降低及红细胞免疫粘附抑制因子活性增强，红细胞免疫粘附功能低下。本研究提示脑梗死患者红细胞免疫功能下降，为探讨动脉粥样硬化性脑梗死的发病与防治途径提供了依据。     

恶性血液病患者红细胞免疫粘附功能的观察

恶性血液病患者红细胞免疫粘附功能的观察广东省人民医院血液内科杜欣本文采用红细胞Ｃ３ｂ受体花环试验方法，测定了３１例恶性血液病患者红细胞膜Ｃ３ｂ受体活性，以反映红细胞的免疫粘附功能。结果表明，上述恶性血液病患者红细胞膜Ｃ３ｂ受体活性均低于正常对照组（Ｐ...     

促红细胞生成素对慢性肾功能衰竭患者免疫功能的影响

对３６例慢性肾功能衰竭（ＣＲＦ）患者应用促红细胞生成素（ＥＰＯ）治疗前后检测红细胞免疫功能及中性粒细胞吞噬功能，粘附率，结果发现ＥＰＯ治疗后ＣＲＦ患者红细胞Ｃ３ｂ受体花环率、红细胞Ｉｃ花环率、中性粒细胞吞噬功能，粘附率均较治疗前明显升高。认为ＥＰＯ可以明显的改善ＣＲＦ患者的免疫功能。     

Kupffer cell complement receptor clearance function and host defense

Kupffer cells are well known to be important for normal host defense function. The development of methods to evaluate the in vivo function of specific receptors on Kupffer cells has made it possible to assess the role of these receptors in host defense. The rationale for studying complement receptors is based on the proposed important role of these receptors in host defense and on the observation that the hereditary deficiency of a complement receptor is associated with recurrent severe bacterial infections. The studies reviewed here demonstrate that forms of injury that are associated with depressed host defense including thermal injury, hemorrhagic shock, trauma, and surgery also cause a decrease in complement receptor clearance function. This decrease in Kupffer cell receptor clearance function was shown not to be the result of depressed hepatic blood flow or depletion of complement components. Complement receptor function was also depressed following the phagocytosis of particulates that are known to depress Kupffer cell host defense function. Endotoxemia and bacteremia also were associated with a depression of complement receptor function. Complement receptor function was experimentally depressed in uninjured animals by the phagocytosis of IgG-coated erythrocytes. There was a close association between the depression of complement receptor clearance function and increased susceptibility to the lethal effects of endotoxin and bacterial infection. These studies support the hypotheses that complement receptors on Kupffer cells are important for normal host defense and that depression of the function of these receptors impairs host defense.     

Decrease of Fc gamma and C3b receptor-bearing granulocytes and of T lymphocytes in myelomatosis

18 patients with myelomatosis had lower percentages of granulocytes bearing receptors for Fc gamma (47.6%) and C3b (43.0%) than controls (80.4% and 75.0%). The percentage of T lymphocytes was decreased in patients when untreated sheep erythrocytes were used as indicator cells. Patients with high serum IgG levels had lower percentages of T lymphocytes. There was no significant difference in receptor profile between treated and untreated patients. The decrease in Fc gamma and C3b receptor-bearing granulocytes in myelomatosis is probably not due to serum or plasma factors since (a) the distribution of receptor-bearing lymphocytes was not different from that of the controls; (b) extra washings of cells or overnight incubation did not enhance the percentage of receptor positive cells; and (c) incubation of normal granulocytes in sera or plasma from myelomatosis patients did not cause a more pronounced reduction in the proportions of Fc gamma of C3b receptor-bearing cells than incubation in normal sera or plasma.     

CD44-mediated phagocytosis induces inside-out activation of complement receptor-3 in murine macrophages

Diverse receptors, including Fcgamma receptors and beta(2) integrins (complement receptor-3 [CR3], CD11b/CD18), have been implicated in phagocytosis, but their distinct roles and interactions with other receptors in particle engulfment are not well defined. CD44, a transmembrane adhesion molecule involved in binding and metabolism of hyaluronan, may have additional functions in regulation of inflammation and phagocytosis. We have recently reported that CD44 is a fully competent phagocytic receptor that is able to trigger ingestion of large particles by macrophages. Here, we investigated the role of coreceptors and intracellular signaling pathways in modulation of CD44-mediated phagocytosis. Using biotinylated erythrocytes coated with specific antibodies (anti-CD44-coated erythrocytes [Ebabs]) as the phagocytic prey, we determined that CD44-mediated phagocytosis is reduced by 45% by a blocking CD11b antibody. Further, CD44-mediated phagocytosis was substantially (42%) reduced in CD18-null mice. Immunofluorescence microscopy revealed that CD11b is recruited to the phagocytic cup. The mechanism of integrin activation and mobilization involved activation of the GTPase Rap1. CD44-mediated phagocytosis was also sensitive to the extracellular concentration of the divalent cation Mg(2+) but not Ca(2+). In addition, buffering of intracellular Ca(2+) did not affect CD44-mediated phagocytosis. Taken together, these data suggest that CD44 stimulation induces inside-out activation of CR3 through the GTPase Rap1.     

Erythroid Fc-IgG and complement receptor expression: a study of normoblastic and megaloblastic human bone marrows

Using a standardized rosetting technique with IgG-coated ox erythrocytes, avid IgG (Fc) receptors were demonstrated on red cell precursors. The proportion of receptor-positive cells in normal marrows was highest in early precursors and appeared to be lost with maturation. In megaloblastosis, the absolute percentage of early precursors increase, but there is an even greater increase in the proportion of receptor-positive cells. It is proposed that this reflects the degree of maturation arrest. The specificity of the receptor was confirmed by inhibition studies with aggregated human IgG. In contrast, the expression of the C3b "immune adherence" receptor, assessed by IgM-C3b-coated ox erythrocytes, was seen to increase with erythroid maturation. Early megaloblasts, especially in severe megaloblastosis, showed a marked decrease in C3b receptor activity, again in proportion to the level of maturation arrest. The significance and possible function of these receptors is discussed.     

Neutrophil surface markers in patients with acute leukemia

The presence of complement and Fc receptors on neutrophils from patients with acute leukemia was investigated at different stages of the leukemic process. Both Fc receptors (Fc-H and Fc-R) and one complement receptor (C3d) were normal when patients were studied at diagnosis, in relapse, and in remission. In contrast, the C3b receptor was significantly reduced on te neutrophils at the time of diagnosis, but returned to normal levels when patients entered remission. Variable amounts of C3b activity were observed in patients relapse, with approximately one-half of the patients showing decreased C3b activity. To determine whether the reduction inC3b receptors was specific for patients at diagnosis, three patients were studied at different times during their diseases. Normal receptor levels were detected in these patients during remission, but the C3b receptor was markedly reduced at diagnosis and at relapse.     

肿瘤坏死因子增强巨噬细胞杀伤约氏疟原虫的观察

目的 :观察肿瘤坏死因子 ( TNF)对巨噬细胞 ( MΦ)表面受体表达及吞噬功能的影响 ,探讨 TNF体内杀伤疟原虫机制。方法 :以感染约氏疟原虫的 BAL B/ c小鼠为动物模型 ,将不同浓度的 TNF与小鼠腹腔 MΦ体外培养 5h后 ,加入感染红细胞 ,观察 MΦ对感染红细胞的吞噬率 ,将 TNF作用后的 MΦ用 m PAP超微半定量法测定 Fc受体 ,YC花环法测定 C3b受体。结果 :TNF能够增加 MΦ 对感染红细胞的吞噬率 ,其作用与 TNF剂量呈正相关。TNF可增加正常及感染鼠MΦ 表面 Fc受体和 C3b受体的表达。结论 :TNF在感染小鼠体内可能调节 MΦ 表面受体的表达并增加其吞噬疟原虫的功能     

Ligand-receptor interactions in the phagocytosis of virulent Streptococcus pneumoniae by polymorphonuclear leukocytes

We used polyclonal and monoclonal antibodies to neutrophil complement receptors CR1 and CR3 to assess the role of these receptors in the phagocytosis of virulent Streptococcus pneumoniae serotypes 3, 6A, and 14, which bear accessible C3 ligands covalently bound to the polysaccharide capsule. When the iC3b receptor (CR3) on normal polymorphonuclear leukocytes (PMNLs) was blocked by the monoclonal antibody OKM10, phagocytosis of pneumococcal serotypes 6A and 14 (which bear exclusively iC3b) was inhibited 50%-80% in pooled human serum and completely in nonimmune serum. Blockade of the PMNL C3b receptor (CR1) failed to inhibit phagocytosis for serotypes 6A and 14. For serotype 3, which bears C3b and C3d (as well as iC3b) on the capsule, CR3-mediated phagocytosis accounted for only 20% of the uptake; again, there was no evidence for CR1-mediated phagocytosis. The iC3b ligand elicited consistently greater release of superoxide, myeloperoxidase, and lactoferrin than did C3b. The iC3b/CR3 interaction is thus the primary trigger for phagocytosis of iC3b-bearing pneumococci and for stimulation of intracellular bactericidal processes.     

Naturally occurring anti-band-3 antibodies and complement together mediate phagocytosis of oxidatively stressed human erythrocytes.

Treatment of erythrocytes with the thiol-specific oxidant azodicarboxylic acid bis(dimethylamide) (diamide) enhances their phagocytosis by adherent monocytes. Phagocytosis of diamide-treated erythrocytes required that the cells were opsonized with whole serum, since complement inactivation abolished phagocytosis. Opsonization with whole serum containing 20-100 times the physiological concentration of naturally occurring anti-band-3 antibodies enhanced phagocytosis of diamide-treated erythrocytes. High inputs of anti-band-3 also restored phagocytosis of erythrocytes that had been incubated with complement-inactivated serum. Elevated concentrations of anti-spectrin antibodies were ineffective in whole and complement-inactivated serum. Specific recognition of diamide-treated erythrocytes by anti-band-3 antibodies may be due to generation of anti-band-3 reactive protein oligomers on intact diamide-treated erythrocytes. Generation of such oligomers was dose-dependent with respect to diamide. Bound anti-band-3 alone was not sufficient to mediate phagocytosis. It resulted in deposition of complement component C3b on the cells through activation of the alternative complement pathway in amounts exceeding that of bound antibodies by two orders of magnitude. Thus, anti-band-3 and complement together mediate phagocytosis of oxidatively stressed erythrocytes, which stimulate senescent erythrocytes with respect to bound antibody and complement.     

Surface markers of human eosinophils

Peripheral blood eosinophils from patients with eosinophilia and from healthy subjects were studied for surface immunoglobulins, receptors for the Fc region of IgG, complement receptors, and spontaneous rosette formation with sheep and mouse erythrocytes. Eosinophils were found to have receptors for complement and for aggregated IgG, and to have the same two types of complement receptors as do lymphocytes and monocytes. Immune adherence type receptors were specific for C4 or C3b, while C3d receptors were specific for C3d but unreactive with C4. Eosinophils differed from fully mature neutrophils in that the former had C3d receptors and relatively weak immune adherence (C4 or C3b) receptors, while the later did not have the C3d receptors and had strong immune adherence receptors. Eosinophil phagocytosis of complement-receptor bound erythrocytes was dependent on the presence of IgG in the antibody coating the red blood cells; this requirement for IgG resembled that found in neutrophil phagocytosis. No surface Ig or spontaneous erythrocyte rosette formation was observed with eosinophils.     

The effect of immune serum and complement on the in vitro phagocytosis of Babesia rodhaini

The effect of immune serum and complement on the in vitro phagocytosis of Babesia rodhaini was investigated. Infected erythrocytes and parasites released from erythrocytes by lysis were phagocytosed by mouse peritoneal macrophages in vitro when the infected erythrocytes or parasites were exposed to hyperimmune B. rodhaini serum. Complement, in the presence of immune serum, did not reproducibly enhance phagocytosis of infected erythrocytes or parasites alone. When adjusted for its effect on normal erythrocytes and normal serum, complement generally inhibited rather than enhanced phagocytosis. When coupled with other published data, our data suggest that the activation of the immune system in vivo against this species of Babesia involves a series of mechanisms of which phagocytosis is but one.