支原体肺炎肺外损伤患儿T细胞亚群、IFNγ、TNFα的变化及意义

目的 探讨支原体肺炎肺外损伤患儿细胞免疫、细胞因子状况和胸腺肽的治疗效果。方法 采用流式细胞仪和酶标仪检测31例支原体肺炎肺外损伤组患儿急性期、恢复期血中CD3CD4、CD8、CD4／CD8干扰素γ（IFNγ）、肿瘤坏死因子α（TNFα水平，并与支原体肺炎组比较。结果 ①急性期支原体肺炎肺外损伤组和支原体肺炎组比较，CD3、CD4显著降低（P〈0．05），TNFα显著升高（P〈0．01），CD8、IFNγ无统计学意义（P〉0．05）；②支原体肺炎肺外损伤组急性期和4周后比较，CD3、CD4、IFNγ升高（P〈0．05），TNFα显著降低（P〈0．01），CD8无变化。用胸腺肽治疗患者以上指标变化更明显。结论 支原体肺炎肺外损伤患儿细胞免疫功能低于支原体肺炎患儿；细胞因子中TNFα早期升高，而IFNγ不明显；恢复期TNFα下降，而IFNγ升高明显。用胸腺肽治疗能缩短病程。     

细胞内游离Ca2+在发育中大鼠皮层神经元无镁诱导惊厥性损伤中的作用

目的: 观察细胞内游离Ca2+([Ca2+]i)在培养的不同发育阶段皮层神经元无镁诱导惊厥性损伤中的作用,探讨惊厥性脑损伤年龄依赖性的可能机制.方法:体外培养6 d、17 d的胚胎大鼠皮层神经元用无镁细胞外液处理3 h,或于无镁处理前用NMDA(N-甲基-D-门冬氨酸)受体拮抗剂或Ca2+通道阻滞剂预处理,用MTT代谢率测定的方法检测神经元损伤,以Fluo-3作标记用激光共聚焦显微镜扫描的方法检测[Ca2+]i.结果:体外培养6 d、17 d的神经元单纯无镁组MTT代谢率较同期对照组降低.应用MK-801 10 μmol*L-1、AP-5 50 μmol*L-1、尼莫地平10 μmol*L-1预处理后再给无镁处理,培养6 d、17 d的神经元MTT代谢率均不同程度高于同期单纯无镁组.培养6 d、17 d的神经元相对荧光强度之间差异有显著性,两者与基线荧光强度比较差异亦有显著性.应用上述各种拮抗剂后,[Ca2+]i改变的峰值均明显低于同期单纯无镁组.结论: 在体外不同发育阶段的神经元,短暂无镁处理诱导惊厥样放电所引起的神经元线粒体功能损伤以及[Ca2+]i改变程度不同.这种[Ca2+]i改变的年龄依赖性可能是惊厥导致神经元损伤的年龄依赖性的机制之一.NMDA受体-Ca2+通道激活是导致这种[Ca2+]i改变及神经元损伤的关键环节.     

Role of Integrin CD103 in Promoting Destruction of Renal Allografts by CD8+ T Cells

Infiltration of CD8(+)TCRalphabeta(+) T-effector populations (CD8 effectors) into graft epithelial compartments has long been recognized as a key lesion in progression of clinical renal allograft rejection. While the afferent phase of allograft immunity is increasingly well-defined, the efferent pathways by which donor-reactive CD8-effector populations access and ultimately destroy the graft renal tubules (rejection per se) have received remarkably little attention. This is an important gap in our knowledge of transplantation immunology, because epithelial compartments comprise the functional elements of most commonly transplanted organs including not only kidney, but also liver, lung, pancreas, and intestine. Furthermore, there is increasing evidence that attack of graft epithelial elements by CD8-effector populations not only causes short-term graft dysfunction but is also a major contributor to development of chronic allograft nephropathy and late graft loss, which now represent the salient clinical problems. Recent studies of the T-cell integrin, alpha(E)beta(7) (CD103), have provided insight into the mechanisms that promote interaction of CD8 effectors with graft epithelial compartments. The purpose of this communication is to review the known properties of the CD103 molecule and its postulated role in the efferent phase of renal allograft rejection.     

胶片剂量测量和验证方法的研究

目的设计和实现基于通用激光扫描仪的胶片剂量测量和验证系统。方法采用胶片饱和冲洗、非线性光学校正、多分辨率阈值滤波、离散傅里叶逆变换图像复原等方法,消除了普通扫描仪用于胶片剂量学定量处理中的各种伪影、噪声和畸变;采用过响应系数校正方法消除测量胶片对低能散射光子的过响应,改善了胶片剂量测量的准确性;采用γ结合NAT指标的方法对放疗计划进行二维定量验证,给出可视化图形表达和具有定量数据的验证结果。结果和三维水箱系统、VeriSoft胶片测量系统相比较,研制系统对放疗剂量的测量结果在±2%内符合一致,对IMRT放疗计划的定量验证结果在±3%内符合一致。结论该系统能够实现对放疗剂量的高精度测量和对适形调强放疗计划剂量的可靠验证。     

Oral administration of an edible-mushroom-derived protein inhibits the development of food-allergic reactions in mice

BACKGROUND: Food allergy is a common disease without effective treatment. Since strict elimination of food allergens may be difficult, strategies for effective intervention are urgently needed. OBJECTIVE: The aim was to investigate the prophylactic use of orally administrated FIP-fve, an immunomodulatory protein isolated from the edible mushroom Flammulina velutipes, in a murine model of food allergy. METHODS: BALB/c mice were immunized twice intraperitoneally with ovalbumin (OVA), at an interval of 2 weeks. Before and during each period of immunization, FIP-fve (200 microg per mouse) or phosphate-buffered saline was given orally every other day with a total of five doses. Then OVA-specific antibodies and cytokine profiles were determined. Subsequently, the mice were orally challenged with OVA. Symptoms of anaphylaxis, levels of plasma histamine, and histology of intestines were examined. RESULTS: Mice receiving oral FIP-fve treatment during sensitization to OVA had an impaired OVA-specific IgE response with a Th1-predominant cytokine profile. These mice were protected from systemic anaphylaxis-like symptoms induced by subsequent oral challenge with OVA. CONCLUSION: Oral administration of FIP-fve has a Th1-skewing effect on the development of the allergen-specific immune response, and may serve the purpose of immunoprophylaxis for food allergy and other allergic diseases.     

100例SARS患者外周血T淋巴细胞亚群分析

目的 :探讨SARS患者外周血T淋巴细胞亚群变化。方法 :采用流式细胞仪检测10 0例SARS住院患者外周血T淋巴细胞亚群。结果 :与正常组比较 ,SARS组白细胞总数显著下降 ,淋巴细胞百分数和绝对数显著下降 ,粒细胞绝对数显著下降 ,CD3 、CD4 、CD8 细胞绝对数显著下降 ,CD4 细胞百分数 ,CD8 细胞百分数及CD4 /CD8 比值差异无统计学意义。比较SARS患者各病程CD3 、CD4 、CD8 ,于病程第一至第三周较第四周下降明显 (P <0 .0 5 ) ,病程第一至第三周之间差别无显著性 (P >0 .0 5 ) ;结论 :SARS患者外周血T淋巴细胞亚群的变化对阐明SARS的发病机制有一定意义。     

保肾口服液影响IgA肾病小鼠T细胞增殖及分泌IL-2的实验研究

观察保肾口服液对IgA肾病小鼠T细胞^3H-TdR掺入及其分泌IL-2水平的影响，结果表明低、中、高3种浓度的保肾口服液均能显著促进IgA肾病小鼠的自发性和ConA刺激的T细胞^3H-TdR掺入，促进T细胞合成，分泌IL-2，提前给药作用相同。提示保肾口服液有显著增强IgA肾病小鼠细胞免疫功能的作用。     

Differential Expression of Subspecies of Polyomavirus and Murine Leukemia Virus Enhancer Core Binding Protein, PEBP2, in Various Hematopoietic Cells

The core sequence of the enhancer of murine leukemia virus (MuLV) long terminal repeat is highly conserved in a large number of MuLV strains and appears to play an essential role when SL3-3 or Moloney strains induce T cell lymphoma in mice. We found by using the electrophoretic mobility shift assay that a polyomavirus enhancer core-binding protein, PEBP2, bound to this core motif of MuLV. We also noted that PEBP2 in several hematopoietic cell lines derived from B lymphocyte, macrophage and myelocyte lineages migrated significantly faster than the authentic PEBP2 detected in NIH3T3 (ibroblasts. Interestingly, PEBP2 detected in the cell lines of T lymphocyte lineage appeared to contain both types, which were indistinguishable in electrophoretic mobility from those of NIH3T3 and of B lymphocyte, macrophage and myelocyte lineages. The treatment of the nuclear extract containing PEBP2 with phosphatase generated PEBP3, which is a subcomponent of PEBP2 and retained the same DNA-binding specificity as PEBP2. The altered mobility of hematopoietic cell-derived or T lymphocyte-derived PEBP2 was found to be due to the alteration of the mobility of PEBP3. Based on the distinct mobility of PEBP2/3 of T lymphocytes from those of other hematopoietic cells, we discuss the implication of PEBP2 in MuLV-induced T cell leukemia and T cell-specific gene expression.     

Ca2+ mobilization in physiologically stimulated single T cells gradually increases with peptide concentration (analog signaling)

We have investigated Ca²⁺ mobilization in single T cells stimulated with their physiological ligand, i.e. antigenic peptide bound to major histocompatibility complex (MHC) molecules on antigen-presenting cells (APC). Fibroblasts expressing I-E^d class II molecules were pulsed with a peptide derived from the λ2³¹⁵ immunoglobulin light chain. Onto such antigen-pulsed fibroblasts were sedimented cloned Th1 cells loaded with Fura-2. Changes in cytosolic Ca²⁺ concentration in single T cells were continually monitored by use of an imaging system based on fluorometry. Ca²⁺ mobilization was both peptide-specific and MHC-restricted. Within seconds of the initial APC-T cell contact, a Ca²⁺ spike could be observed. The Ca²⁺ response gradually declined over a 25-min period, during which oscillations were noted. Various parameters characterizing the magnitude of the Ca²⁺ response (latency, increase rate, max and mean Ca²⁺ increase, frequency and period of oscillations) all correlated with the amount of peptide used for pulsing the fibroblasts. Thus, Ca²⁺ mobilization in single T cells appears not to be an all or none phenomenon. Rather, activation is incremental (analog signaling), the degree of Ca²⁺ mobilization probably being related to the number of stimulatory peptide-MHC complexes on the surface of the APC. The extent of calcium mobilization and lymphokine production (interleukin (IL)-2, IL-3, interferon-γ) correlated, at least at the population level.