多抗甲素对荷S180瘤小鼠红细胞免疫功能的影响

观察了荷Ｓ１８０瘤小鼠红细胞免疫功能的改变及多抗甲素治疗对其红细胞免疫功能的影响。试验分三组，即正常组、肿瘤组、多抗甲素治疗肿瘤组。荷瘤１０天后，检测各组红细胞免疫功能各项指标。结果显示：荷瘤小鼠的红细胞免疫功能较正常对照组全面下降（Ｐ＜０．０１）。表现为：１．ＲＢＣ－Ｃ３ｂ受体花环率下降，ＲＢＣ－ＩＣ花环率上升，为继发性红细胞Ｃ３ｂ受体免疫粘附功能下降。２．血清中红细胞Ｃ３ｂ受体免疫粘附促进因子活性下降，而抑制因子活性上升。３．红细胞免疫粘附肿瘤细胞能力下降。经多抗甲素治疗后，可使荷瘤小鼠红细胞抗肿瘤免疫功能较未治疗组全面上升（Ｐ＜０．０１）。提示荷瘤小鼠的红细胞免疫功能低下，多抗甲素抗肿瘤活性与提高红细胞免疫功能有关     

原发性肝癌患者红细胞免疫粘附肿瘤细胞能力与红细胞CR1基因型及活性相关性分析

目的　研究原发性肝癌患者红细胞免疫粘附肿瘤细胞能力与红细胞ＣＲ１ 基因组密度多态性及活性的相关性。方法　采用ＰＣＲ 和Ｈｉｎｄ Ⅲ酶切技术测定红细胞ＣＲ１ 基因组密度多态性变化,同时用ＥＬＩＳＡ 和肿瘤红细胞花环试验测定红细胞ＣＲ１ 活性,并进行比较。结果　原发性肝癌患者红细胞ＣＲ１ 基因型点突变比率（４３－６ ％ ） 明显上升,与正常人（２０ ％ ） 相比,差异有显著性（ Ｐ＜０－０５） ;原发性肝癌患者３ 种ＣＲ１ 基因型的红细胞ＣＲ１ 活性都明显低于正常人（ Ｐ＜ ０－０１ 或 Ｐ＜０－０５） 。活性变化也不同。结论　原发性肝癌患者红细胞ＣＲ１ 活性及免疫粘附肿瘤细胞能力下降可分为三种不同类型,即原发型、获得型和混合型。     

肺癌患者红细胞CR1基因密度型分布与红细胞免疫变化的研究

目的检测３２例肺癌患者红细胞ＣＲ１基因密度型分布、红细胞免疫粘附肿瘤细胞功能及ＳＯＤ酶活性、β－内啡肽含量。方法ＰＣＲ法检测红细胞ＣＲ１基因密度多态性；红细胞花环法检测红细胞免疫粘附肿瘤细胞能力；放免法测定ＳＯＤ酶活性；ＲＩＡ法测定β－内啡肽含量。结果经与３１例正常人比较显示：肺癌患者ＣＲ１基因密度多态性分布与正常人不一致（χ２＝３．１９，Ｐ＜０．０５）；红细胞免疫功能及ＳＯＤ酶活性较正常人明显降低（Ｐ＜０．０１）；β－内啡肽较正常人明显升高（Ｐ＜０．０１）。同时还发现肺癌患者的红细胞粘附肿瘤细胞功能与ＳＯＤ酶活性呈正相关（ｒ＝０．３９．Ｐ＜０．０５）。结论肺癌患者红细胞免疫功能低下；ＳＯＤ酶活性降低；β－内啡肽含量升高有部分与红细胞ＣＲ１基因密度型改变有关     

肿瘤红细胞免疫新进展

肿瘤红细胞免疫是红细胞免疫的新课题。新近研究表明：红细胞主要通过ＣＲ１与各种肿瘤细胞发生免疫粘附，在血循环中旁路激活并粘附Ｃ３ｂ、Ｃ４ｂ，可激活红细胞膜上过氧化物酶等活性杀伤癌细胞。同时具有促进淋巴细胞粒细胞对肿瘤细胞的粘附，促进粒细胞吞噬，在肿瘤免疫中具有调控作用，患肿瘤患者红细胞免疫表现为继发性缺陷，检测红细胞免疫在临床上具有重要意义     

胸腺素促进红、白细胞免疫粘附功能的实验研究

通过红、白细胞免疫粘附混合花环证明胸腺素可促进红、白细胞补体受体活性。通过肿瘤红细胞花环试验证明胸腺素可促进红细胞免疫粘附肿瘤细胞。继用抗ＣＲ１单克隆抗体阻断实验证明红细胞免疫粘附肿瘤细胞系红细胞ＣＲ１的作用。     

肺癌患者红细胞CR1基因密度型分布与红细胞免疫变？…

目的 检测３２例肺癌患者红细胞ＣＲ１基因密度型分布，红细胞免疫粘附肿瘤细胞功能及ＳＯＤ酶活性、β－内啡肽含量。方法 ＰＣＲ法检测红细胞ＣＲ１基因密度多态性，红细胞花环法检测红细胞免疫粘附肿瘤细胞能力；放免法测定ＳＯＤ酶活性；ＲＩＡ法测定β－内啡肽含量。     

晚期肝癌患者红细胞与淋巴细胞粘附肿瘤细胞能力的研究

目的　探讨晚期肝癌患者红细胞和淋巴细胞对肿瘤细胞的免疫粘附能力。方法　采用红细胞和淋巴细胞免疫粘附肿瘤细胞及红细胞促淋巴细胞免疫粘附肿瘤细胞实验方法 ,对 43例晚期肝癌患者进行研究。结果　晚期肝癌患者红细胞和淋巴细胞免疫粘附肿瘤细胞能力都明显下降(P <0 0 1) ,特别是淋巴细胞对肿瘤细胞的免疫粘附功能下降更明显。肝癌患者和正常人的红细胞对自身淋巴细胞具有免疫粘附促进作用 ,但肝癌患者红细胞对自身淋巴细胞的免疫粘附促进作用明显低于正常人 (P <0 0 5 )。结论　红细胞、淋巴细胞免疫粘附肿瘤功能试验 ,可考虑作为肝癌患者免疫功能测定指标之一 ,红细胞免疫粘附功能的变化在晚期肝癌疾病发展及预后中具有一定作用     

SLE及RA患者的红细胞免疫功能

红细胞表面具有１型补体受体（ＣＲ１）、Ⅲ型补体受体ＣＲ３、ＣＤ５８、ＣＤ５９、ＩＬ－８受体和ＳＯＤ酶等。人类红细胞膜上的ＣＲ１为糖肽，其主要配体是Ｃ３ｂ、Ｃ４ｂ、ｉＣ３ｂ和ｉＣ４ｂ。Ｃ３ｂ受体具有免疫粘附功能。人体清除循环免疫复合物（ＣＩＣ）的功能主要是红细胞，其清除作用较具有免疫和防御机能的白细胞高５００～１０００倍。因此，红细胞免疫粘附（ＲＣＩＡ）功能的变化与疾病的关系日益受到重视。我们采用酵母菌花环试验，测定了２７例ＳＬＥ和３１例ＲＡ患者外周血ＲＢＣ－Ｃ３ｂＲ花环率及ＲＢＣ－ＩＣＲ花环率，…     

白细胞免疫粘附肿瘤细胞实验研究

根据白细胞有补体受体可免疫粘附补体致敏肿瘤细胞的原理而设计白细胞免疫粘附肿瘤细胞花环实验。用于研究红细胞免疫调节作用，以及脑外伤淋巴细胞免疫功能的变化，显示有实用价值。     

晚期肝癌患者红细胞与淋巴细胞粘附肿瘤细胞能力的 …

目的 探讨晚期肝癌患者红细胞和淋巴细胞对肿瘤细胞的免疫粘附能力。方法 采用红细胞和淋巴细胞免疫粘附肿瘤细胞及红细胞促淋巴细胞免疫粘附肿瘤细胞实验方法,对４３例晚期肝癌患者进行研究。结果 晚期肝癌患者红细胞和淋巴细胞免疫粘附肿瘤细胞能力都明显下降（Ｐ〈０．０１）,特别是淋巴细胞对肿瘤细胞的免疫粘附功能下降更明显。肝癌患者和正常人的红细胞对自身淋巴细胞具有免疫粘附促进作用,但肝癌患者红细胞对自身淋巴细     

胃癌患者红细胞与白细胞免疫功能的相关性研究

胃癌患者红细胞与白细胞免疫功能的相关性研究郭峰，李淑德，谢苏庆，沈茜第二军医大学附属长海医院免疫室上海２００４３３摘要＊８本文表明胃癌患者红细胞与白细胞免疫功能明显低于良性胃病患者（Ｐ＜０．０１）。胃癌根治术后及中药治疗（如云芝多糖）能促进红细胞免疫...     

紫外线照射全血对红细胞免疫功能及脂质过氧化的影响

为了研究Ｂ波段紫外线（ＵＶＢ）照射全血对红细胞免疫功能及全血抗氧化能力的影响，利用１．５Ｊ／ｃｍ２的ＵＶＢ对全血进行照射，结果发现照射后红细胞Ｃ３ｂ受体花环促进率（ＲＦＥＲ）明显升高（Ｐ＜０．０５），而红细胞Ｃ３ｂ受体（ＲＣＲ）花环率升高更为明显（Ｐ＜０．０１），红细胞免疫复合物（ＲＢＣ－ＩＣ）花环率及与红细胞Ｃ３ｂ受体花环抑制率（ＲＦＩＲ）在照射前后无明显改变（Ｐ＞０．０５），红细胞超氧化物歧化酶（ＳＯＤ）活性在照射后明显升高（Ｐ＜０．０１），而血浆中丙二醛（ＭＤＡ）含量无明显改变（Ｐ＞０．０５）。说明紫外线照射能改善红细胞免疫功能及全血的抗氧化能力。     

Adherence to human monocytes of red cells from autoimmune haemolytic anaemia and red cells sensitized with alloantibodies

Red cells sensitized with autoantibodies are able to adhere in vitro to autologous monocytes and monocytes from healthy individuals. A direct relationship between the degree of sensitization and the percentage of rosettes was not observed, while such a correlation was found if red cells sensitized with anti-Rh alloantibodies were used. Sometimes the adherence of red cell from AIHA was observed although the sensitization was weaker than that of the control erythrocytes sensitized with anti-CD serum which did adhere to monocytes. In patients with AIHA some relation was found between the adherence assay, haemolysis in vivo and treatment with prednisone.     

Red Cell Immune Adherence (Rcia): Its Application in Cancer and Autoimmune Disease

A rosette technique is described which measures the relative activity of the red cell immune adherence (RCIA) receptor. Antibody-coated sheep red cells, in the presence of complement, adhere to human red cells and thus form mixed human-sheep red cell aggregates (RR-rosettes). The percentage of human red cells adhering to one or more sheep red cells is used as the parameter of RCIA activity.

The RCIA receptor activity of 23 cancer patients, 13 patients with autoimmune diseases, and 39 age-matched control was compared by investigating the ability of human red cells to adhere to antibody and complement coated sheep red cells and thus form RR-rosettes. We noticed a decrease in the percentage of RR-rosettes forming cells in cancer patients (p < 0.0005). In contrast, patients with autoimmune disease showed a significant increase in RR-rosettes when compared to age-matched controls (p < 0.05). Thus malignancy and autoimmune disease are associated with surface changes of erythrocytes, specifically those of the receptors, which are responsible for the immune adherence reaction.     

红细胞免疫功能的测定在恶性血液病病人中的应用及其临床意义

目的 :了解恶性血液病病人红细胞免疫功能状况。方法 :采用红细胞酵母菌花环试验检测 40例恶性血液病患者红细胞免疫功能。结果 :红细胞C3b受体花环率 (RCR)及红细胞促中性粒细胞吞噬率(ERPN)显著下降 ,红细胞免疫复合物花环率 (RICR)和C3b受体花环抑制率 (RFIR)显著升高 ,而红细胞C3b受体花环增强率 (RFER)显著降低。结论 :恶性血液病患者存在红细胞免疫功能继发性损害 ,急性白血病缓解期红细胞免疫功能有所恢复 ,但仍较对照组低 (P <0 .0 5 )。恶性淋巴瘤及多发性骨髓瘤缓解红细胞免疫功能基本恢复正常     

SETDB1: A perspective into immune cell function and cancer immunotherapy

Oncogene SET Domain Bifurcated 1 (SETDB1)/ESET, an H3K9 methyltransferase, was originally discovered over two decades ago; however, its function in the immune response was not first reported until 2011. SETDB1 immune functions include B cell maturation, T cell activity regulation, and immune escape in cancer cells. In B lymphocytes, SETDB1 mediates the transition from pro-B to pre-B cells and represses endogenous retroviruses (ERV) to encourage B cell lineage differentiation and maturation. SETDB1 alters T cell function by methylating IL-2 and IL-17 promoters and mediating T cell lineage commitment and development. In addition, SETDB1 plays a critical role in ERV silencing within a variety of immune cells, which can indirectly weaken the immune response. Although SETDB1 is critical for normal immune cell function, overexpression in cancer cells negatively impacts immune cell fights against cancer through decreased tumour immunogenicity. Within cancer cells, SETDB1 overexpression represses production and infiltration of antitumour immune cells, mediates immune escape through TE and ERV silencing, represses the type I interferon pathway, and interferes in immune checkpoint blockade (ICB) outcomes by regulation of PD-L1 expression and IFN signalling. In this review, we further discuss the immunological mechanisms of SETDB1 in normal and cancerous cells and its implications in cancer immunotherapy.     

Promising approaches in cancer immunotherapy

Immunotherapy is a promising field, which enhances and harnesses the powers of the host immune system against cancer and in recent years, has become a major application of the fundamental research of cancer immunology. Cancer immunotherapy is often more targeted than non-specific therapy approaches, including radiotherapy or chemotherapy, as the immune system can be trained to remember cancer cells, highlighting a durable approach that can be maintained after the treatment completion. Immunotherapy functions by directing the immune system to attack the tumour cells via targeting tumour antigens, also enhancing the existing anti-tumour immune responses. Current strategies include non-specific immunotherapy, cancer vaccines, oncolytic virus therapy, monoclonal antibodies, immune checkpoints and T cell therapy. The combination of effective approaches can increase the immunotherapy efficacy, leading to durable anti-tumour immune responses. This review will discuss the immunotherapy approaches, particularly immune checkpoints and T cell therapy, which are the most common clinical applications in cancer immunotherapy.     

Immunology in the clinic review series; focus on cancer: double trouble for tumours: bi-functional and redirected T cells as effective cancer immunotherapies

Cancer is one of the most important pathological conditions facing mankind in the 21st century, and is likely to become the most important cause of death as improvements continue in health, diet and life expectancy. The immune response is responsible for controlling nascent cancer through immunosurveillance. If tumours escape this control, they can develop into clinical cancer. Although surgery and chemo- or radiotherapy have improved survival rates significantly, there is a drive to reharness immune responses to treat disease. As T cells are one of the key immune cells in controlling cancer, research is under way to enhance their function and improve tumour targeting. This can be achieved by transduction with tumour-specific T cell receptor (TCR) or chimaeric antigen receptors (CAR) to generate redirected T cells. Virus-specific cells can also be transduced with TCR or CAR to create bi-functional T cells with specificity for both virus and tumour. In this review we outline the development and optimization of redirected and bi-functional T cells, and outline the results from current clinical trials using these cells. From this we discuss the challenges involved in generating effective anti-tumour responses while avoiding concomitant damage to normal tissues and organs.     

The immunosuppressive tumour network: myeloid‐derived suppressor cells,regulatory T cells and natural killer T cells

Myeloid‐derived suppressor cells (MDSC) and regulatory T (Treg) cells are major components of the immune suppressive tumour microenvironment (TME). Both cell types expand systematically in preclinical tumour models and promote T‐cell dysfunction that in turn favours tumour progression. Clinical reports show a positive correlation between elevated levels of both suppressors and tumour burden. Recent studies further revealed that MDSCs can modulate the de novo development and induction of Treg cells. The overlapping target cell population of Treg cells and MDSCs is indicative for the importance and flexibility of immune suppression under pathological conditions. It also suggests the existence of common pathways that can be used for clinical interventions aiming to manipulate the TME. Elimination or reprogramming of the immune suppressive TME is one of the major current challenges in immunotherapy of cancer. Interestingly, recent findings suggest that natural killer T (NKT) cells can acquire the ability to convert immunosuppressive MDSCs into immunity‐promoting antigen‐presenting cells. Here we will review the cross‐talk between MDSCs and other immune cells, focusing on Treg cells and NKT cells. We will consider its impact on basic and applied cancer research and discuss how targeting MDSCs may pave the way for future immunocombination therapies.     

Expression of VCAM-1, ICAM-1, E- and P-selectin and tumour-associated macrophages in renal cell carcinoma

AIMS: Neoangiogenesis is accompanied by an increase in endothelial surface, which can support infiltration by immune cells depending on adhesion molecule expression. Therefore, the expression of cell adhesion molecules on microvessels and epithelial cells was analysed in renal cell carcinomas as compared to tumour-free tissue. METHODS AND RESULTS: PECAM-1, CD34, ICAM-1, VCAM-1, VLA-4, P- and E-selectin, the macrophage antigens Ki-M1P and Mac-1, and lymphocyte function antigen LFA-1 were identified immunohistochemically. VCAM-1, ICAM-1, and E-selectin were equally or less expressed, whereas P-selectin was increased on microvessels in tumour tissue. The density of VCAM-1-positive tumour microvessels correlated positively with an advanced tumour stage and E- and P-selectin-positive tumour microvessels with the amount of associated macrophages. The expression of ICAM-1 and VCAM-1 on neoplastic epithelia correlated with an increased density of macrophages and a minor degree of tumour differentiation. CONCLUSIONS: The positive correlation of macrophage infiltration and expression of cell adhesion molecules on tumour microvessels and epithelia with minor tumour differentiation and an advanced stage indicates that adhesion molecule expression is not associated with an effective antitumour function of macrophages