病毒性心肌炎患者多项免疫参数分析

本文对比检测急性期与恢复期病毒性心肌炎患者多项免疫指标，结果揭示急性期病毒性心肌炎患者中性粒血胞的吞噬和杀菌功能明显低下，而恢复期患者的中性粒细胞功能基本恢复至正常人水平。急性期和恢复期病人的ＮＫ细胞活性明显低于健康人，尤以急性期下降更为明显。不同期患者的外周血中Ｔ和Ｂ淋巴细胞百分率则无异常变化，与健康人组近似。患者静息或诱导后表达ｍＩＬ—２Ｒ的活化Ｔ淋巴细胞数明显高于健康人组，而血中ＳＩＬ—２Ｒ水平与正常值近似。此外，两组患者ＩｇＧ、Ａ、Ｍ水平均有不同程度的明显升高，在恢复初期仍保持较高的ＩｇＭ水平。上述结果揭示急性期病毒性心肌炎患者中性粒细胞和ＮＫ细胞活性下降、三种Ｉｇ升高，确有免疫水平异常现象，但与疾病的因果关系有待探讨。     

慢性病毒性心肌炎患者体内的α干扰素及其他免疫功能的动态研究

本文对22例慢性病毒性心肌炎、9例急性病毒性心肌炎痊愈者和正常人进行了α-干扰素诱生能力和免疫指标的测定。检查发现慢性组的α-干扰素诱生能力和淋巴细胞PHA转化率较急性病毒性心肌炎痊愈组和正常对照组为低。而IgM和单份血清柯萨奇B1-6型病毒中和抗体效价≥1:32者较后二组为高。上述结果提示慢性病毒性心肌炎可能由于免疫异常引起病毒反复活动或持续存在所引起。故治疗方面尚应考虑提高机体的防御病毒能力,并提出若在心肌炎的急性期进行干扰素能力检测,低于正常给予干扰素或其他增加诱生干扰素能力的药物,有可能避免部分急性病毒性心肌炎患者进入慢性阶段。     

病毒性心肌炎患者外周血单核细胞来源DCs的功能研究

目的:体外诱导病毒性心肌炎患者外周血单核细胞来源的DCs(Mo-DCs),并探讨其功能状态的变化,为寻求病毒性心肌炎的致病机制和新的治疗途径提供实验依据。方法:无菌分离18例临床病毒性心肌炎患者及20例健康志愿者外周血单核细胞,分别加入粒细胞巨噬细胞集落刺激因子(granulocyte-macrophage colony-stimulating factor,GM-CSF)和白细胞介素4(IL-4)诱导外周血Mo-DCs,应用免疫荧光标记技术、流式细胞分析和酶联免疫吸附试验(ELISA)等方法比较病毒性心肌炎患者和健康志愿者外周血Mo-DCs的表型、吞噬能力和表达细胞因子的差异。结果:病毒性心肌炎患者外周血Mo-DCs表达较高水平的CD83、CD80、CD86和MHCⅡ,但是吞噬能力下降,并且分泌较高水平的TNFα-(P<0.01)和IL-12(P<0.01),可以更有效地刺激T淋巴细胞增殖。结论:病毒性心肌炎患者外周血Mo-DCs处于较成熟功能状态,且表达较高水平的IL-12和TNFα-。进而有可能通过调节T细胞、NK细胞和巨噬细胞发挥效应而在病毒性心肌炎的发生发展中起到举足轻重的作用。     

病毒性心肌炎患者血清可溶性白介素2受体水平变化的临床观察

目的 :探讨病毒性心肌炎患者血清白介素 2受体 (ＳＩＬ - 2Ｒ)水平变化及意义。方法 :33例均为住院患者 ,男 1 9例 ,女 1 4例 ,平均年龄 1 8 2± 6 7,诊断标准均符合 1 999年 5月全国心肌炎心肌病学术研讨会镇江会议提出的修订意见标准。对照组 1 6例为本院健康献血者 ,女 7例 ,男 9例 ,平均年龄 2 3 4± 5 8。采用酶联双抗体夹心法及直接花环法测定病毒性心肌炎患者急性期和恢复期血清可溶性白介素 2受体(ＳＩＬ - 2Ｒ)水平及Ｔ淋巴细胞亚群含量 (ＣＤ3～8) ,以观察其在病毒性心肌炎时的变化。结果 :病毒性心肌炎患者急性期ＳＩＬ - 2Ｒ含…     

人类肿瘤抗原对活性E花环形成细胞的激活作用

为了研究肿瘤抗原,并寻找肿瘤的免疫诊断方法,我们用胃癌、肺癌、食管癌抗原分别作用子胃癌(14例)、肺癌(16例)、食管癌(9例)、非肿瘤疾患(6例)和正常人(10例)的淋巴细胞,观察肿瘤抗原对活性E花环(Ea花环)试验的影响。实验结果是:肿瘤病人的淋巴细胞与相应抗原温育后形成Ea花环的百分率比不加抗原的对照管显著增多(P<0.01),而正常人的淋巴细胞与抗原温育后形成Ea花环的百分率和不加抗原的对照管相比较没有显著增多,或相反地出现减少现象。肿瘤病人的淋巴细胞与不相应的抗原温育后也未见Ea花环显著增多。如以Ea花环增多率16％为界限,即16％以上者为阳性,16％以下者为阴性,则肿瘤病人的阳性率为92.3％(36/89),10例正常人全部阴性,6例非肿瘤疾病患者中1例阳性。为了得到准确的实验结果,本试验在操作技术上必须严格细致。     

黄芪加美乐心治疗病毒性心肌炎疗效观察

目的 :病毒性心肌炎是青壮年较常见的心肌疾病 ,近年来其发病率有上升趋势。自 1997年以来 ,我们在抗病毒等综合治疗的基础上 ,用黄芪加美乐心静脉点滴治疗心肌炎 ,取得良好的疗效 ,现将结果报告如下。方法 :6 5例病毒性心肌炎患者均符合“1987年心肌炎心肌病座谈会”制订的病毒性心肌炎诊断标准 ,治疗组 34例 ,其中男 2 1例 ,女 13例 ,年龄 16 - 5 6岁 ,平均年龄 36岁 ,对照组 31例 ,其中男 2 2例 ,女 9例 ,年龄 18- 5 2岁 ,平均 35岁 ,治疗组与对照组在年龄、症状、心电图及心肌酶学、心功能等方面均无明显差异。 6 5例病毒性心肌炎患者随…     

病毒性心肌炎患者细胞免疫功能检测的临床意义

目的:探讨病毒性心肌炎患者细胞免疫功能检测的临床意义.方法:选择本院2008-01/2009-12收治的病毒性心肌炎患者75例作为实验组,以67例健康者作为对照组,分别在入院时和入院后24 h内静脉采血,对治疗前后T细胞亚群、自然杀伤细胞(NK)活性及肿瘤坏死因子(TNF)进行检测和分析.结果:与入院时比较,入院24 h后实验组外周血T淋巴细胞亚群CD3、CD4、CD8及CD4/CD8均有所提高,且CD3、CD4及CD4/CD8差异均具有统计学意义(P<0.05),但仍略低于对照组,而差异不具有统计学意义;与此同时,与入院时比较,入院24 h后实验组NK及TNF均有所提高,差异均具有统计学意义(P<0.05),但仍略低于对照组,而差异不具有统计学意义.结论:更加深入地探讨病毒性心肌炎患者的免疫损伤机制将有助于更好地指导治疗,而且具有重要的临床意义.     

自身免疫性甲状腺疾病患者外周血淋巴细胞端粒长度的研究

目的：研究自身免疫性甲状腺疾病（ATD）患者外周血淋巴细胞端粒长度的变化。方法：用流式原位杂交法检测38例ATD患者和48例健康对照者外周血淋巴细胞的端粒长度。结果：患者组外周血淋巴细胞端粒长度明显短于健康对照组（P＜0．001）,端粒长度与病程、发病时间、甲状腺激素水平不相关。健康对照组端粒长度随年龄增加而变短,病人组端粒长度与年龄不相关。结论：ATD病人的外周血淋巴细胞端粒长度比正常人短,且与年龄不相关,提示其外周血淋巴细胞复制、分裂增多及凋亡异常。     

淋巴细胞化学发光的研究进展

淋巴细胞化学发光(Ly-CL)是淋巴细胞活化的早期事件之一。本文系统阐述了Ly-CL 的细胞学和生物化学基础;Ly-CL 与淋巴细胞活化的关系;归纳总结了Ly-CL 的理论和实际意义。Ly-CL 反映了淋巴细胞活化早期的氧化代谢活性及活性氧自由基的生成,并依赖于胞浆游离Ca~(2+)浓度的增加。Ly-CL 测定法可为研究淋巴细胞分化、活化和巨噬细胞、病毒、药物等对淋巴细胞的作用以及NK 细胞的功能提供一种简便、快速的有效手段。     

常见胃肠道疾病患者空腹血清胃泌素RIA

我院于1993年测定飞129例常见胃肠道疾病患者的空腹血清胃泌素,并与31例正常人对照组进行了比较,现将结果报告如下。 对象和方法 一、正常对照组:共31例(男21,女10),年龄在18～60岁之间,系本院健康体检者,均无上消化道不适及器质性病变。 二、胃肠道疾病组:均为我院住院病人,共179例,其中非溃疡性消化不良(NUD)患者25例(男18,女7),年龄21～60岁,有慢性持续性中上腹不适、疼痛、饱胀及烧心等,并经上消化道钡透或胃镜、B超检查排除消化性溃疡、肿瘤及肝胆胰疾病,符合     

Non-HLA Lymphocyte Cytotoxins in Various Diseases

Cold non-HLA lymphocyte cytotoxins were found to be principally reactive against B lymphocytes. These antibodies were studied in 1335 patients with a wide range of diseases such as systemic lupus erythematosus (SLE), rheumatoid arthritis (RA), scleroderma, Hashimoto's disease, asthma, diabetes, lymphoma, psoriasis, leukemia, multiple sclerosis, and also in healthy donors. Antibodies reactive to B lymphocytes in the cold or warm test conditions were not directed against HLA specificities. Since B lymphocytes differ from T lymphocytes principally in that they have surface immunoglobulin, it is postulated that at least one target antigen of cold lymphocyte cytotoxins is not a virus, infectious agent, or a genetically determined structural antigen, but, rather, simply immunoglobulin.     

Production of Specific Antibodies by Cerebrospinal Fluid Lymphocytes in Patients with Herpes Zoster, Mumps Meningitis and Herpes Simplex Virus Encephalitis

We applied a new method consisting of short-term culture (18 h) of lymphocytes from cerebrospinal fluid (CSF-L) and peripheral blood (PBL) in viral antigen-coated ELISA plates and subsequent measurement of IgG and IgM antibodies bound to antigen. Utilizing mumps virus, herpes simplex virus (HSV), varicella zoster virus (VZV), and measles virus as antigens, we demonstrated production by CSF-L of antibodies against the aetiological agent only in all patients with mumps meningitis and HSV encephalitis and also in all patients with herpes zoster without central nervous system (CNS) symptoms. This might be considered as direct evidence that specific antibodies are produced within the CNS in inflammatory nervous system diseases. CSF-L usually produced higher amounts of antibodies than the corresponding number of PBL. In comparison with concentrations of free antibodies determined in parallel, our method had higher specificity and sensitivity and gave more precise information about the antibody response in infections of the nervous system.     

Secondary prophylaxis for herpes zoster wi oral acyclovir in HIV patients]

We studied 39 AIDS patients from 1989 to 1996, with previous history of herpes zoster. Twelve of them received acyclovir (ACV) secondary prophylaxis. There were 31 males and 8 females, mean age 33.9 years (19-60) during first herpes zoster. Transmission was sexual in 71.8%. Among these 39 patients, 78 herpes zoster episodes occurred. Median CD4 lymphocytes was 18/mm3 (0-232) among the 12 patients with ACV prophylaxis. Mean posology of ACV was 2,400 mg (1,600-4,000) per day, during mean 10 months (median 4 months). ACV prophylaxis was used because of high frequence of herpes zoster (more than 4) (4 cases), neurologic complications in 4 cases (1 myelitis, 1 myeloradiculitis, 1 vascularitis and 1 meningo-encephalitis), disseminated herpes zoster in 4 cases and one hyperalgic zoster. Ten from these 12 patients occurred no zoster recurrence. Among patients without prophylaxis, zoster recurrences were more frequent at 12 months (68% versus 22% among patients with prophylaxis). This prophylaxis seems to be interesting, particularly in deep immunocompromised patients (CD4 < 50/mm3) with serious herpes zoster or frequent recurrences (more than 4). However, since protease inhibitors treatments, zoster incidence is decreasing in HIV+ patients. This prophylaxis will probably be less usefull than before.     

Effect of viral load on the outcome of herpes zoster

Varicella-zoster virus (VZV) is a member of the Herpesviridae family, primary infection with which causes varicella, more commonly known as chicken pox. Characteristic of members of the alphaherpesvirus subfamily, VZV is neurotropic and establishes latency in sensory neurons. Reactivation of VZV causes herpes zoster, also known as shingles. The most frequent complication following zoster is chronic and often debilitating pain called postherpetic neuralgia (PHN), which can last for months after the disappearance of a rash. During episodes of acute zoster, VZV viremia occurs in some, but not all, patients; however, the effect of the viral load on the disease outcome is not known. Here we describe the development of a highly specific, sensitive, and reproducible real-time PCR assay to investigate the factors that may contribute to the presence and levels of baseline viremia in patients with zoster and to determine the relationship between viremia and the development and persistence of PHN. VZV DNA was detected in the peripheral blood mononuclear cells (PBMCs) of 78% of patients with acute zoster and in 9% of healthy asymptomatic blood donors. The presence of VZV in the PBMCs of patients with acute zoster was independently associated with age and being on antivirals but not with gender, immune status, extent of rash, the age of the rash at the time of blood sampling, having a history of prodromal pain, or the extent of acute pain. Prodromal pain was significantly associated with higher baseline viral loads. Viral load levels were not associated with the development or persistence of PHN at 6, 12, or 26 weeks.     

Detection of antibody to varicella-zoster virus by competitive and IgM-antibody capture immunoassay

A simple, sensitive, and specific competitive solid phase immunoassay for antibody to varicella-zoster virus (anti-VZV) is described. The assay uses reagents that can easily be prepared and is sparing of viral antigen. Using a solid phase coated with sheep IgG from a serum raised against human mu-Fc, the same reagents will accurately detect anti-VZV IgM. The competitive assay divided sera from children from adults into immune and nonimmune groups that closely correlated with a history of previous VZV illness. It was not affected by the presence or absence of antibody to other herpes viruses. The IgM antibody capture assay demonstrated the presence of anti-VZV IgM in sera from patients with both varicella and zoster and gave negative results in patients with infections unrelated to VZV and in healthy blood donors.     

Alteration of immunoregulatory mechanisms during cytomegalovirus mononucleosis: effect of in vitro culture on lymphocyte blastogenesis to viral antigens

Immunoregulation of lymphocyte blastogenesis was studied in 13 patients with acute-phase cytomegalovirus (CMV) mononucleosis and 9 of these patients during the convalescent phase of the illness. Peripheral blood mononuclear leukocytes from acute-phase patients displayed depressed uptake of [3H-]thymidine in response to the lectin-mitogen concanavalin A (Con A) and immune-specific viral antigens (CMV, herpes simplex virus (HSV), mumps virus) compared with convalescent patients or normal donors. Removal of plastic-adherent cells from the patients' samples resulted in further depression of lymphocyte blastogenesis to Con A and CMV and HSV antigens, suggesting a helper function for the predominantly monocytic, adherent cell population in this response. Preliminary culture of mononuclear leukocytes from acute-phase patients for 18 hr at 37 degrees C resulted in significantly enhanced blastogenesis to Con A. In sharp contrast, lymphocyte blastogenesis to viral antigens was not significantly enhanced after preculture. These results suggest that different mechanisms are operative in immunoregulation of lymphocyte recognition responses to the polyclonal activator Con A and immune-specific viral antigens during human CMV infection.     

Secretion of cytokines,histamine and leukotrienes in chronic urticaria

BACKGROUND: Approximately 35-40% of patients with chronic urticaria have an IgG autoantibody to the IgE receptor which can activate basophils and mast cells so that they release histamine. In this study we assessed the cytokine profile present in chronic urticaria sera, and then measured cytokine and leukotriene release from basophils and mast cells upon incubation with chronic urticaria sera. Finally we assessed cytokine expression at the single-cell level and characterized the T cell subpopulations involved in their production. We chose IL-4 as representative of Th2 lymphocytes and IFN-gamma for Th1 lymphocytes. METHODS: We analyzed IL-4, IL-5 and IFN-gamma in 60 chronic urticaria sera versus 51 controls. Sera were incubated with purified human basophils and cutaneous mast cells and the release of histamine, IL-4 and leukotrienes (C(4), D(4), E(4)) was quantitated. Immunoblotting was performed to identify IgG antibody to FcepsilonRIalpha, alpha subunit. We measured intracellular cytokine production in peripheral blood mononuclear cells of 17 chronic urticaria patients compared to 50 healthy controls. RESULTS: We found higher IL-4 levels (p = 0.028) in the sera of chronic urticaria patients (1.03 pg/ml) versus healthy donors (0.20 pg/ml) but no difference between urticaria sera and atopic control sera (0.52 pg/ml). We did not detect IFN-gamma or IL-5 in any serum. However, sera that activated basophils so that they released histamine also produced leukotriene and IL-4, and leukotriene production by cutaneous mast cells and basophils was closely correlated. However, there was no correlation between immunoblotting and the functional ability to induce either histamine or IL-4. After stimulating with PMA-ionomycin we found significant differences in CD4+ lymphocyte production of IL-4 and IFN-gamma with no differences in CD8+ lymphocyte production of either cytokine. CONCLUSION: Our data support the presence of basophil and mast cell activators in the sera of patients with chronic urticaria which can lead to the production of leukotrienes and IL-4 in addition to the histamine. IL-4 levels are similar to those seen in atopic subjects. We found that CD4+ T cells from patients with chronic urticaria are activated and tend to produce higher cytokine levels than CD4+ T cells from healthy controls. There were no differences when cytokine production by CD8+ lymphocytes was similarly assessed. These results are consistent with the histology found in biopsies of chronic urticaria lesions, where a CD4+-predominant infiltrate is found with cytokine production suggesting either a Th0 response or a mixture of Th1 and Th2 lymphocytes.     

PPD-induced viral antibody production in human blood lymphocytes.

The ability of purified protein derivative of tuberculin (PPD) to induce polyclonal antibody production in cultures of human blood lymphocytes was studied. IgG and IgM were determined by the enzyme-linked immunosorbent assay (Elisa). PPD induced both IgM and IgG production, with a predominance of IgM. PPD usually stimulated a stronger IgM response but a weaker IgG response than did pokeweed mitogen (PWM). Supernatants of PPD- or PWM-stimulated lymphocyte cultures were tested for antibodies to morbilli, rubella and herpes simplex by Elisa. PPD as well as PWM induced viral antibody production in lymphocytes of donors who had serum antibodies to the corresponding viral antigens. Production of viral antibodies of IgG class but not of IgM class was demonstrated. The PPD-induced antibody response was T cell-dependent.     

Determination of specific IGA antibodies to varicella zoster virus by immunoperoxidase assay.

An indirect peroxidase technique was developed for determination of IgA antibodies to varicella zoster virus (VZV). The antigen consisted of acetone-fixed trypsinised VZV-infected cells. Rabbit antihuman IgA peroxidase conjugate was used to detect human IgA antibodies bound to viral antigen. In parallel IgG antibodies to VZV were determined by an immunoperoxidase antibody to membrane antigen (IPAMA) technique. Varicella zoster virus IgA antibodies were detected in all five varicella and seven zoster patients. No VZV IgA antibodies (less than 2) were detected in 45 healthy control sera. Neither were they found in paired sera of five patients with herpes simplex infection, five patients with human cytomegalovirus infection and two patients with Epstein-Barr virus infection. Application of immunoperoxidase IgA technique in serodiagnosis of primary and reactivated VZV infections is discussed.