凋亡细胞促进狼疮性BXSB小鼠发病的研究

目的 探讨凋亡细胞在系统性红斑狼疮发病中的作用。方法 将体外诱导的凋亡胸腺细胞经腹腔注射给同基因同性别的正常Ｃ５７小鼠和具有狼疮倾向的雌雄ＢＸＳＢ小鼠;检测血清中ＬｇＭ和ＩｇＧ类型的抗ｄｓＤＮＡ抗体和抗ｓｓＤＮＡ抗体的水平,尿蛋白浓度以及肾脏中ＩｇＧ类型免疫复合物的沉积。结果 用凋亡腺细胞免疫后,诱导Ｃ５７小鼠产生ＩｇＧ类型的抗ｄｓＤＮＡ抗体和抗ｓｓＤＮＡ抗体;相比之下,诱导雌性ＢＸＳＢ小鼠产生更高水平的ＩｇＧ类型抗ｄｓＤＮＡ抗体和抗ｓｓＤＮＡ抗体;并且使雄性ＢＸＳＢ小鼠的尿蛋白浓度显著升高。结论 凋亡细胞具有免疫原性,它可能是狼疮性ＢＸＳＢ小鼠体内自身抗原的主要来源;狼疮性遗传因素和Ｙａａ基因能促进凋亡细胞的免疫原性和增强凋亡细胞的致肾炎作用。     

活性DNA诱导抗核抗体及系统性红斑狼疮样综合征

目的 寻找系统性红斑狼疮真正的核成分免疫原。方法 从ＣｏｎＡ活化的脾淋巴细胞中提取ＤＮＡ，然后同系免疫ＢＡＬＢ／ｃ小鼠，用ＥＬＩＳＡ方法测定ＩｇＧ类抗ｄｓＤＮＡ，抗组蛋白抗体，用免疫荧光法检测抗核抗体核型和免疫复合物沉积，用免疫印迹法测定抗可溶性抗原抗体，用考马斯亮蓝法检测抗体阳性的动物尿蛋白含量。结果 活性ＤＮＡ能诱导抗ｄｓＤＮＡ、抗组蛋白等多种抗核抗体生成，且能诱发同系小鼠产生ＳＬＥ样综合征。     

弓形虫ROP1基因真核表达重组质粒免疫小鼠后的免疫应答

目的： 用构建的弓形虫ｐｃＤＮＡ３－ＲＯＰ１ 真核表达重组质粒, 直接免疫小鼠, 观察其所诱导的细胞及体液免疫反应。方法： 碱裂解法大量制备ｐｃＤＮＡ３－ＲＯＰ１ 质粒, 经肌肉注射免疫ＢＡＬＢ／ｃ 小鼠, 每鼠注射１００ μｇ,２ ｗ ｋ 后同量加强免疫１ 次, 以ｐｃＤＮＡ３ 空质粒及生理盐水组为对照。分别于免疫后３０ ｄ、５０ ｄ、７０ ｄ 共３ 次用ＭＴＴ 法测定小鼠脾脏Ｔ 淋巴细胞增殖活性及ＮＫ 细胞活性; 用间接免疫荧光抗体法测定Ｔ淋巴细胞亚群数目;ＥＬＩＳＡ 法测定ＩｇＧ 抗体滴度。结果： 用ｐｃＤＮＡ３－ＲＯＰ１ 质粒免疫小鼠３０ ｄ 后, 脾脏明显增大; 免疫组脾淋巴细胞增殖活性明显高于生理盐水及空质粒对照组。ＮＫ 细胞杀伤活性３ 次的测定结果免疫组均高于对照组。Ｔ 细胞亚群, ＣＤ４＋ 细胞数与对照组相比较无明显变化, 而ＣＤ８＋ 细胞数显著增高。血清抗体ＩｇＧ７０ ｄ 内检测结果, 与对照组相比较, 无明显增高; 而免疫后９０ ｄ 检测明显增高, 抗体滴度１∶１００。结论： 用ｐｃＤＮＡ３－ＲＯＰ１ 重组质粒ＤＮＡ免疫小鼠, 可诱导产生细胞及体液免疫应答。     

空肠弯曲菌蛋白抗原分析

超声粉碎和高速离心获得Ｃ．ｊ－Ｓ１３１ｌｙｓａｔｅ，ＳＤＳ－ＰＡＧＥ显示位于１０－９２ＫＤ间２４条蛋白条带，薄层扫描发现４３ＫＤ蛋白是菌体最主要成份，其次是１５ＫＤ和１７ＫＤ蛋白。Ｗｅｓｔｅｒｎｂｌｏｔｔｉｎｇ发现Ｃ。ｊ－Ｓ１３１ｌｙｓａｔｅ中４３ＫＤ蛋白抗原性最强，也最早诱导相应抗体产生。用凝胶过滤和液相制备型等电聚焦分离获得了纯化的９２ＫＤ、４３ＫＤ、１５ＫＤ三种蛋白。本文结果为进一步研究空弯菌诱致自身免疫综合征的分子机理打下了基础。     

抗dsDNA抗体抗原识别及致病性的分子基础

抗双链ＤＮＡ抗体 (ｄｓＤＮＡ)是系统性红斑狼疮 (ＳＬＥ)的特异性和致病性抗体 ,几乎存在于所有病人血清中 ,并与临床表现密切相关。目前 ,越来越多的证据表明它是特异性抗原驱动的结果。本文就近年来对于抗ｄｓＤＮＡ抗体本身的结构特点、识别的抗原结构以及其致病机制的研究进展作一综述。1　抗ｄｓＤＮＡ抗体的分子结构抗ｄｓＤＮＡ抗体具有许多对外来抗原再次应答的特征 ,如ＩｇＭ向ＩｇＧ的类型转换以及体细胞突变。在抗ｄｓＤＮＡ抗体中 ,Ｖ区基因突变积累的结果常使其产生ｄｓＤＮＡ特异性和 /或增强结合ｓｓＤＮＡ、ｄｓＤＮＡ的…     

恶性疟原虫FCC-1/HN株pcDNA_3-Pfs25重组质粒在小鼠体内的免疫应答

目的　探讨恶性疟原虫ＤＮＡ 疫苗在小鼠体内的免疫反应。方法　将恶性疟原虫ＦＣＣ－ １／ＨＮ株有性期阶段的重组质粒ｐｃＤＮＡ３－ Ｐｆｓ２５ 经骨骼肌途径注射ＢＡＬＢ／ｃ小鼠,对注射部位的骨骼肌进行了预处理,即于注射前７ｄ 先在左后肢股四头肌注射０．５％ 盐酸布比卡因５０μｌ,注射深度为２ｍ ｍ 。观察免疫后不同时间点小鼠血清ＩｇＧ抗体滴度、脾淋巴细胞增殖反应、ＣＤ４＋ ／ＣＤ８＋ Ｔ细胞亚群比值和ＮＫ 细胞杀伤活性的变化。结果　１）重组质粒ｐｃＤＮＡ３－ Ｐｆｓ２５ 经肌肉注射途径免疫小鼠后,机体ＩｇＧ抗体滴度增高、特异性Ｔ淋巴细胞增殖反应增强、ＣＤ８＋ Ｔ细胞亚群比值增高以及ＮＫ细胞杀伤活性增强。２）肌肉注射为一有效的ＤＮＡ疫苗免疫途径。结论　采用编码有性期基因的重组质粒ｐｃＤＮＡ３－ Ｐｆｓ２５ 经骨骼肌注射途径免疫小鼠,能诱导机体有效的体液免疫、细胞免疫和ＮＫ细胞杀伤活性。本研究为恶性疟ＤＮＡ疫苗的研究提供了免疫学实验依据     

脑囊虫病人血清中循环抗原特性的分析

本研究用免疫印渍法，以三种抗血清为探针，对脑囊虫病人血清中的循环抗原、囊虫头节和体壁抗原及囊液抗原进行了比较观察。结果表明循环抗原与两种囊虫抗原相同的组分有４个ＫＤ数为７５、４３、４０、２３的多肽；仅与虫头及囊壁相同的抗原为６５ＫＤ多肽；仅与囊液相同的多肽为８５、１９ＫＤ二组分。这显示循环抗原主要来源于虫囊的全部结构；循环抗原可诱发三种特异性免疫球蛋白的产生，依次为ＩｇＧ、ＩｇＡ及ＩｇＭ。可诱发ＩｇＧ的循环抗原多肽是８５、５３、４３、４０、３１、１９、１８．５及１７．５ＫＤ多肽；可诱发ＩｇＡ抗体的抗原多肽ＫＤ数为６５、４９、４３、４０及３５的组分；而ＩｇＭ特异性抗体产生于ＫＤ数为７５、４３、４０及３１的多肽。三种抗体血清用于检测血清中的循环抗原都显示出良好的应用价值。免疫兔血清的敏感性与特异性均不亚于单克隆抗体的识别结果。４３及４０ＫＤ多肽是循环抗原中的主要组分，是诊断的重要指标。     

抗核抗体的检测方法及其临床意义

抗核抗体的检测方法及其临床意义张少凌关键词抗核抗体；检测方法；临床意义抗核抗体（ａｎｔｉｎｕｃｉｅａｒａｎｔｉｂｏｄｙ，ＡＮＡ）是一类以真核细胞核成分为靶抗原自身抗体的总称。根据其核成分中靶抗原的不同，可分为①抗ＤＮＡ抗体，包括ｄｓ－ＤＮＡ、ｓｓ－Ｄ...     

肺孢子虫病实验与临床研究 Ⅱ．免疫印迹试验检测人血清肺孢子虫抗体

采用ＳＤＳ－ＰＡＧＥ分析鼠源卡氏肺孢子虫包囊可溶性抗原呈现２０条以上多肽区带，主带分子量分别为＞１００、８５－９４、６７、５２和３４ｋＤａ。ＥＩＴＢ检测表明重庆地区健康人血清中存在识别１１０、１０５、８５、６７、５２和４６ｋＤａ的ＩｇＧ型抗体，抗体阳性率为５６．７％（５９／１０４）。其中８５ｋＤａ抗原能与抗人源肺孢子虫单克隆抗体２Ｇ２起反应。健康人血清抗８５ｋＤａ抗原的抗体阳性率为３７．５％（３９／１０４），但ＩｇＭ型抗体均为阴性。另外检测７例确诊的卡氏肺孢子虫病患者，４例血清ＩｇＧ型抗体阳性，其中３例抗８５ｋＤａＩｇＧ型抗体阳性。     

用基因工程表达的Cag-A和Hsp-58抗原检测人血清幽门螺杆菌抗体

１材料和方法１．１材料消化门诊及住院患者共计１２１例其中３３例分别进行ＣａｇＡ和Ｈｓｐ－５８基因Ｈｐ抗体的检测（２９例与常规尿素酶法进行比较）;８８例血清标本用ＣａｇＡ及Ｈｓｐ－５８抗原混合包被药盒进行检测１．２方法Ｃａｇ－Ａ和Ｈｓｐ－５８抗原购自ＭＩＣＲＯＧＥＮ生物技术有限公司,酶标抗体为羊抗人ＩｇＧ（ＤＡＫＯ,ｐ２１４）常规尿素酶检测（ＨＰＵ）试剂盒由协和医药集团提供;基因工程表达的ＣａｇＡ及Ｈｓｐ－５８抗原混合包被试剂盒由北京贝尔生物快检技术有限公司提供Ｃａｇ－Ａ和ｈｓｐ－５８抗原经ＳＤＳ…     

The predominance of IgG3 and IgM isotype antimitochondrial autoantibodies against recombinant fused mitochondrial polypeptide in patients with primary biliary cirrhosis

Autoantibodies against inner mitochondrial membrane proteins are a hallmark of primary biliary cirrhosis. Specifically, these antimitochondrial autoantibodies recognize two polypeptides of approximately 70 and 52 kD, respectively. Although the specificity of antimitochondrial autoantibodies has been studied for the past 2 decades, the complementary DNA encoding the major primary biliary cirrhosis-specific 70 kD antigen has only recently been cloned. The availability of the recombinant autoantigen has resulted in the development of a highly sensitive and specific ELISA to detect antimitochondrial autoantibodies and to determine their immunoglobulin isotypes. We report herein that IgG3 is the predominant isotype of antimitochondrial autoantibodies in a group of 74 primary biliary cirrhosis patients. This finding is significant in light of the genomic immunoglobulin in heavy chain gene arrangement. Ninety-three per cent of primary biliary cirrhosis patients possessed IgG3 antimitochondrial autoantibodies with titers of 1:10(3) or higher; 32% of these patients possessed titers of 10(4), 29% at 10(5) and 7% at 10(6). IgM antimitochondrial autoantibodies were next most prevalent; 63% of the patients were positive and 50% of these patients showed titers of 10(3), 43% at 10(4) and 6% at 10(5). Other isotypes were present but in much lower titer and occurrence. Isotypes of antimitochondrial autoantibodies reactive to the 52 kD antigen were also determined using immunoblotting techniques. The predominance of IgG3 and IgM were similarly observed. Finally, the serum immunoglobulin isotype levels of primary biliary cirrhosis patients were compared with healthy normal adults by radial immunodiffusion. Serum IgG3 and IgM were very elevated in primary biliary cirrhosis; with IgG3 at 5.5-fold and IgM at 4.3-fold above normals.(ABSTRACT TRUNCATED AT 250 WORDS)     

Accelerated development of IgG autoantibodies and autoimmune disease in the absence of secreted IgM

Individuals with systemic lupus erythematosus and rheumatoid arthritis are characterized by the presence of high levels of circulating IgM and IgG autoantibodies. Although IgG autoantibodies often are pathogenic, the role of IgM autoantibodies in autoimmune disease is not clear. Using mice that are unable to secrete IgM but are able to express surface IgM and IgD and to secrete other classes of immunoglobulins, we examined the effect of the absence of secreted IgM in the development of IgG autoantibodies and autoimmune disease in lupus-prone lymphoproliferative (lpr) mice. Compared with regular lpr mice, lpr mice that lack secreted IgM developed elevated levels of IgG autoantibodies to double-stranded DNA and histones and had more abundant deposits of immune complexes in the glomeruli; they also suffered more severe glomerulonephritis and succumbed to the disease at an earlier age. Similarly, the absence of secreted IgM also resulted in an accelerated development of IgG autoantibodies in normal mice. These findings suggest that secreted IgM, including IgM autoantibodies produced naturally or as part of an autoimmune response, may lessen the severity of autoimmune pathology associated with IgG autoantibodies.     

Complement deposition in autoimmune hemolytic anemia is a footprint for difficult-to-detect IgM autoantibodies

In autoimmune hemolytic anemia autoantibodies against erythrocytes lead to increased clearance of the erythrocytes, which in turn results in a potentially fatal hemolytic anemia. Depending on whether IgG or IgM antibodies are involved, response to therapy is different. Proper identification of the isotype of the anti-erythrocyte autoantibodies is, therefore, crucial. However, detection of IgM autoantibodies can be challenging. We, therefore, set out to improve the detection of anti-erythrocyte IgM. Direct detection using a flow cytometry-based approach did not yield satisfactory improvements. Next, we analyzed whether the presence of complement C3 on a patient’s erythrocytes could be used for indirect detection of anti-erythrocyte IgM. To this end, we fractionated patients’ sera by size exclusion chromatography and tested which fractions yielded complement deposition on erythrocytes. Strikingly, we found that all patients with C3 on their erythrocytes according to standard diagnostic tests had an IgM anti-erythrocyte component that could activate complement, even if no such autoantibody had been detected with any other test. This also included all tested patients with only IgG and C3 on their erythrocytes, who would previously have been classified as having an IgG-only mediated autoimmune hemolytic anemia. Depleting patients’ sera of either IgG or IgM and testing the remaining complement activation confirmed this result. In conclusion, complement activation in autoimmune hemolytic anemia is mostly IgM-mediated and the presence of covalent C3 on patients’ erythrocytes can be taken as a footprint of the presence of anti-erythrocyte IgM. Based on this finding, we propose a diagnostic workflow that will aid in choosing the optimal treatment strategy.     

Evidence that human autoimmune thrombocytopenia mediated by both immunoglobulin isotypes IgM and IgG is an independent disease entity

Autoimmune thrombocytopenic purpura (AITP) is a bleeding disorder caused by clonally restricted self-reactive antibodies with specificity for platelet glycoproteins. Anti-platelet autoantibodies in AITP mainly belong to the IgG class. The occurrence of anti-platelet autoantibodies of the IgM isotype has been reported, and AITP is partially mediated by antibodies of both isotypes, IgM and IgG. Using a technique of quantitative immunoblotting of immunoglobulins on self-tissues, followed by multiparametric statistical analysis of the data, we here demonstrate that patients with IgM- and IgG-mediated AITP are readily discriminated from patients with IgM-mediated AITP as well as from patients with IgG-mediated AITP at the basis of self-reactive antibody repertoires of isotypes IgM and IgG toward non-platelet antigens of human origin. Our data suggest that, in view of the important physiological functions of self-reactive antibody repertoires, human AITP mediated by both immunoglobulin isotypes IgG and IgM may be an independent disease entity. The role of autoantibody isotype for the pathophysiology of AITP might currently be underestimated, and diagnostic and therapeutic procedures in AITP might profit from considering autoantibody isotype more carefully.     

Characterization of the humoral immune response against Gnathostoma binucleatum in patients clinically diagnosed with gnathostomiasis

Gnathostomiasis is an emerging systemic parasitic disease acquired by consuming raw or uncooked fresh-water fish infected with the advanced third-stage larvae of Gnathostoma spp. This disease is endemic to the Pacific region of Mexico, and one of its etiologic agents has been identified as Gnathostoma binucleatum. We characterized the humoral immune response of patients clinically diagnosed with gnathostomiasis by detecting total IgM, IgE, and IgG class and subclasses against a crude extract of the parasite by Western blotting. Our results do not show differences in the antigens recognized by IgM and IgE. However, we found that the specific humoral immune response is caused mainly by IgG, specifically IgG4. We found that 43%, 65.2%, 54.1%, and 26.3% of the patients recognize the 37-kD, 33-kD, 31-kD, and 24-kDa antigens, suggesting that the 33-kD antigen is the immunodominant antigen of G. binucleatum.     

Nine-year's follow up on the appearance of autoantibodies in a child with idiopathic thrombocytopenic purpura subsequently developing lupus with central nervous system manifestations]

We describe a 23-year-old female who developed SLE 9 years after asymptomatic idiopathic thrombocytopenic purpura (ITP) with positive antinuclear antibody (ANA). Although the platelet count was normal before the onset of SLE, the titer of ANA was gradually increased and also autoantibodies, including antibodies to SS-A/Ro, single-stranded DNA (ss-DNA) and nuclear ribonucleoprotein (RNP) changed to positive. At 23 years of age, the patient was admitted to our hospital because of fever, butterfly rash and polyarthritis. Anti double-strand DNA (ds-DNA) antibody and anti Smith antigen (Sm) antibody were positive and the platelet count and titer of complements were decreased. The patient was diagnosed as SLE and treated with 60 mg/day of prednisolone. Despite steroid therapy, psychiatric symptoms appeared. Additional treatments with steroid pulse therapy and double filtration plasmaphresis resulted in the improvement of SLE including the central nervous system manifestations. This case suggested that increased titer of ANA and the appearance of antibodies to SS-A, ss-DNA, RNP, ds-DNA and Sm in ITP patients predict the development of SLE. Routine checkup of autoantibodies is needed to manage ITP with positive ANA.     

High diagnostic value of anticalpastatin autoantibodies in rheumatoid arthritis detected by ELISA using human erythrocyte calpastatin as antigen

OBJECTIVE: To develop a quantitative method of measuring autoantibodies against human calpastatin in rheumatoid arthritis (RA) and to determine their diagnostic value compared with other autoimmune and articular diseases. METHODS: We performed a highly sensitive ELISA for IgG and IgM anticalpastatin autoantibodies in human sera using human erythrocyte calpastatin as an antigen. Samples were diluted 1:2000 for the measurement of IgG and 1:400 for IgM. RESULTS: IgG anticalpastatin antibodies were found in the sera of 48 of 58 patients (82.8%) with RA. In contrast, IgG anticalpastatin antibodies were found in the sera of only 2 of 11 (8.3%) patients with osteoarthritis (OA). Compared to sera from patients with other autoimmune diseases, anticalpastatin antibody sensitivity for RA was better than that of systemic lupus erythematosus (5.6%), systemic sclerosis (0%), mixed connective tissue disease (0%), and Sj?gren's syndrome (20%). IgG anticalpastatin antibodies also showed high specificity (96.1%) for RA. Almost 90% of patients with RA were positive for IgG or IgM anticalpastatin antibodies. CONCLUSION: We have developed a simple, sensitive, specific, and quantitative ELISA for anticalpastatin antibodies that may have a high diagnostic value for RA.     

Anticalmodulin autoantibody in liver diseases: a new antibody against a cytoskeleton-related protein

An ELISA has been developed for detection of auto-antibodies against calmodulin. There was a significantly increased frequency (63.1%) of autoantibodies against calmodulin in 103 patients with chronic liver diseases as compared to that (30%) of patients with systemic lupus erythematosus and to that (6.9%) of normal subjects (p less than 0.01). IgG autoantibodies against calmodulin were detected in the patients with acute hepatitis (37.9%), chronic liver disease (45.6%) and also in the patients with systemic lupus erythematosus (30%). IgM autoantibodies against calmodulin were frequently found in patients with liver cirrhosis (52.2%), primary biliary cirrhosis (50%) and autoimmune chronic active hepatitis (38.7%), but rarely in patients with acute hepatitis (13.8%), chronic persistent hepatitis (9.5%) and systemic lupus erythematosus (0%). IgA autoantibodies against calmodulin were frequently found in liver cirrhosis (33.3%), primary biliary cirrhosis (42.9%) and autoimmune chronic active hepatitis (53.6%), but rarely in chronic persistent hepatitis (15.8%), chronic active hepatitis (14.3%) and systemic lupus erythematosus (0%). The occurrences of autoantibodies against calmodulin correlated neither with those of antismooth muscle antibody, antinuclear antibody and antimitochondrial antibody, nor with serum IgG concentrations. Autoantibodies against calmodulin did not cross-react with troponin, myosin light chain, calf thymus DNA and actin. The titer of autoantibodies against calmodulin was decreased by absorption of serum with calmodulin and the liver plasma membrane fraction. The immunoblotting experiment revealed the binding of autoantibodies against calmodulin to calmodulin. IgG fraction from a patient with autoimmune chronic active hepatitis inhibited the activation of phosphodiesterase by calmodulin.(ABSTRACT TRUNCATED AT 250 WORDS)     

Beneficial effects of the anti-oestrogen tamoxifen on systemic lupus erythematosus of (NZBxNZW)F1 female mice are associated with specific reduction of IgG3 autoantibodies

BACKGROUND: Sex hormones have been shown to influence the immune system and to modify the course of autoimmune disorders. OBJECTIVE: To examine the effects of the oestrogen antagonist tamoxifen on the course of systemic lupus erythematosus (SLE) in (NZBxNZW)F1 mice. METHODS: Groups of 8 week old (NZBxNZW)F1 female mice were treated with tamoxifen (800 micro g/mouse; twice a week) or with double distilled water for four months. Mice were evaluated monthly for the presence of autoantibodies directed against DNA and nuclear extract (NE) by enzyme linked immunosorbent assay (ELISA). White blood cells and thrombocytes were quantified by a cell counter and proteinuria by combistix kit. At 6 months of age, all mice that did not die spontaneously were killed and evaluated for the presence of glomerular immune deposits by indirect immunofluorescence assay. IgG isotypes of autoantibodies in the mouse sera and glomeruli were determined by gamma chain specific antibodies. RESULTS: Tamoxifen treatment significantly reduced autoantibody production directed against either NE or DNA. The latter reduction was mainly in autoantibodies of the IgG3 isotype. Furthermore, tamoxifen had significant beneficial effects on the course of SLE in (NZBxNZW)F1 mice. At 6 months of age, 40% of the untreated mice died spontaneously, whereas all the tamoxifen treated mice were still alive. All untreated mice showed severe thrombocytopenia and persistent proteinuria, with diffuse glomerular immune deposits of IgG2a and IgG3 isotypes in their kidneys. In contrast, the tamoxifen treated mice had a normal number of thrombocytes and only minimal proteinuria. Moreover, glomerular immune deposits were detected in <40% of the tamoxifen treated mice. The latter were mainly of the IgG2a but not of the IgG3 isotype. CONCLUSION: The results clearly show the remarkable therapeutic effects of tamoxifen on SLE of (NZBxNZW)F1 female mice and suggest that these beneficial effects are related to the specific reduction of IgG3 autoantibodies.     

Anticardiolipin antibodies in patients with autoimmune diseases: Isotype distribution and clinical associations

Summary A prospective study of IgG and IgM isotypes of anticardiolipin antibodies (aCL) was performed in a series of 167 patients with various autoimmune diseases, including rheumatic and nonrheumatic disorders, and in a group of 100 healthy blood donors. The IgG aCL serum was regarded as positive if a binding index (BI) greater than 2.85 (3.77 SD) was detected and a BI greater than 4.07 (3.90 SD) was defined as positive for IgM aCL. Forty patients (24%) were found to be positive for IgG and/or IgM aCL. IgG aCL were detected in 23% of patients with systemic lupus erythematosus (SLE), in 9% with idiopathic thrombocytopenic purpura, in 7% with progressive systemic sclerosis, and in 6% with dermatomyositis-polymyositis. IgM aCL were present in 43% patients with primary biliary cirrhosis, in 33% with rheumatoid arthritis, in 22% with SLE, and in 8% with giant-cell arteritis. IgG aCL were found to have a significant association with thrombosis and thrombocytopenia, and IgM and aCL with haemolytic anaemia and neutropenia, in SLE but not in the other autoimmune diseases. The identification of these differences in the aCL isotype associations, depending on the autoimmune disorder, may improve the clinical usefulness of these tests.