Clinical immunology and immunopathology最新文献

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Human Neutrophils Express the Prostaglandin G/H Synthase 2 Gene When Stimulated with Bacterial Lipopolysaccharide 细菌脂多糖刺激人中性粒细胞表达前列腺素G/H合成酶2基因
Clinical immunology and immunopathology Pub Date : 1998-06-01 DOI: 10.1006/clin.1998.4545
Mary B. Fasano , Jon D. Wells, Charles E. McCall
{"title":"Human Neutrophils Express the Prostaglandin G/H Synthase 2 Gene When Stimulated with Bacterial Lipopolysaccharide","authors":"Mary B. Fasano ,&nbsp;Jon D. Wells,&nbsp;Charles E. McCall","doi":"10.1006/clin.1998.4545","DOIUrl":"10.1006/clin.1998.4545","url":null,"abstract":"<div><p>Human blood neutrophils (PMN) rapidly release arachidonic acid (AA) from cellular phospholipids when stimulated<em>in vitro</em>with a variety of inflammatory agonists. Free AA is then metabolized via 5′-lipoxygenase to produce bioactive mediators such as leukotriene B<sub>4</sub>and 5-hydroxyeicosatetraenoate. Arachidonic acid can also be metabolized via the cyclooxygenase or prostaglandin G/H synthase (PGHS) pathway to form prostaglandins and thromboxane. We show here that human blood PMN express the PGHS 2 gene when stimulated with bacterial lipopolysaccharide (LPS). PGHS 2 mRNA increases within 30 min after LPS stimulation and PGHS 2 immunoreactive protein is detectable by 5 h. Although PGHS 1 mRNA is detectable in PMN, no immunoreactive protein is observed in either resting or LPS-stimulated cells. Following stimulation with LPS and expression of PGHS 2, PMN increase secretion of prostaglandin E<sub>2</sub>. This phenotypic change in PMN could be an important mechanism for regulating inflammation.</p></div>","PeriodicalId":10683,"journal":{"name":"Clinical immunology and immunopathology","volume":"87 3","pages":"Pages 304-308"},"PeriodicalIF":0.0,"publicationDate":"1998-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1006/clin.1998.4545","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"20565401","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 25
Cell Death and Oxidative Damage in Inflammatory Myopathies 炎症性肌病的细胞死亡和氧化损伤
Clinical immunology and immunopathology Pub Date : 1998-06-01 DOI: 10.1006/clin.1998.4527
Dominique S. Tews, Hans H. Goebel
{"title":"Cell Death and Oxidative Damage in Inflammatory Myopathies","authors":"Dominique S. Tews,&nbsp;Hans H. Goebel","doi":"10.1006/clin.1998.4527","DOIUrl":"10.1006/clin.1998.4527","url":null,"abstract":"<div><p>There is evidence that muscle fibers in denervating disorders and muscular dystrophies undergo apoptosis. In 21 patients with autoimmune inflammatory myopathies, we found no features of muscle fiber apoptosis such as DNA fragmentation or expression of apoptosis-related proteins. However, muscle fibers in myositis displayed distinct up-regulation of inducible and neuronal nitric oxide synthase (NOS). While inducible NOS was distinctly up-regulated on the sarcolemma of all kinds of muscle fibers neuronal NOS displayed increased expression in the sarcoplasm of damaged as well as atrophic muscle fibers. There were no disease-specific patterns in the different myositis subtypes. Enhanced expression of NOS with production of nitric oxide may contribute to oxidative stress mediating muscle fiber damage and muscle fiber necrosis representing the predominant cell death mechanism in myositis. Nevertheless, inflammatory cells displayed numerous DNA-fragmentation-positive nuclei and expression of apoptosis-related proteins indicating that apoptosis plays a role in the regulation of the inflammatory cellular response.</p></div>","PeriodicalId":10683,"journal":{"name":"Clinical immunology and immunopathology","volume":"87 3","pages":"Pages 240-247"},"PeriodicalIF":0.0,"publicationDate":"1998-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1006/clin.1998.4527","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"20564840","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 85
Effect of Aging on Experimental Autoimmune Prostatitis: Differential Kinetics of Development 衰老对实验性自身免疫性前列腺炎的影响:发展的差异动力学
Clinical immunology and immunopathology Pub Date : 1998-06-01 DOI: 10.1006/clin.1998.4534
Gabriel Morón, Belkys Maletto, Andrea Rópolo, Marı́a Cristina Pistoresi-Palencia
{"title":"Effect of Aging on Experimental Autoimmune Prostatitis: Differential Kinetics of Development","authors":"Gabriel Morón,&nbsp;Belkys Maletto,&nbsp;Andrea Rópolo,&nbsp;Marı́a Cristina Pistoresi-Palencia","doi":"10.1006/clin.1998.4534","DOIUrl":"10.1006/clin.1998.4534","url":null,"abstract":"<div><p>We have studied the influence of aging on the kinetics of autoimmune response in Experimental Autoimmune Prostatitis (EAP). EAP was induced in 3- and 12-month-old Wistar rats by i.d. immunization with a saline extract of rat male sex accesory glands (RAG), chemically modified, and emulsioned in CFA. After immunization, 12-month-old rats developed a faster and stronger specific DTH response against RAG and mononuclear infiltration in the prostate. The levels of total IgM and IgG against RAG were lower in 12-month-old rats than in 3-month-old rats, with a prevalence of IgG2a, IgG2b, and IgG2c subclasses in both ages. Immunization stimulated slightly the appearance of specific IgG1 to RAG only in 3-month-old rats but in 12-month-old rats there was no specific IgG1 to RAG. On the other hand, normal 12-month-old rats showed higher levels of some natural antibodies and their thymocytes and peripheral lymphocytes had a diminished proliferative capacity compared to 3-month-old rats. These data demonstrated that 12-month-old rats show parameters of an aged immune system and present an exacerbated autoimmune prostatitis compared with 3-month-old rats.</p></div>","PeriodicalId":10683,"journal":{"name":"Clinical immunology and immunopathology","volume":"87 3","pages":"Pages 256-265"},"PeriodicalIF":0.0,"publicationDate":"1998-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1006/clin.1998.4534","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"20564842","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 10
The Association Between Anti-Ribosomal P Antibodies and Active Nephritis in Systemic Lupus Erythematosus 抗核糖体P抗体与系统性红斑狼疮活动性肾炎的关系
Clinical immunology and immunopathology Pub Date : 1998-06-01 DOI: 10.1006/clin.1998.4541
Vishala Chindalore, Barbara Neas, Morris Reichlin
{"title":"The Association Between Anti-Ribosomal P Antibodies and Active Nephritis in Systemic Lupus Erythematosus","authors":"Vishala Chindalore,&nbsp;Barbara Neas,&nbsp;Morris Reichlin","doi":"10.1006/clin.1998.4541","DOIUrl":"10.1006/clin.1998.4541","url":null,"abstract":"<div><p>Autoantibodies to anti-ribosomal P protein have been recognized in patients with systemic lupus erythematosus (SLE) in widely variable proportions of unselected patients. Presence of anti-ribosomal P antibodies was retrospectively studied in 69 patients with SLE during disease exacerbations and remissions or during continuously active disease. Anti-ribosomal P antibodies were positive in 21/69 patients during active disease, with an overall prevalence of 30.4%. Prevalence in patients with active nephritis was 75.0% (15/20),<em>P</em>value by Fisher's exact test of 8.39 × 10<sup>−7</sup>. In 12/13 patients (92.3%), anti-P disappeared during periods of disease remission,<em>P</em>= 0.0002. In 17/21 patients (81.0%) with anti-ribosomal P antibodies, anti-dsDNA antibodies were also positive. In 47 patients without anti-P, 23/47 (48.9%) were also positive for anti-dsDNA. In 9/12 patients (75.0%) titers of anti-dsDNA antibodies correlated with anti-P during disease exacerbations and remissions,<em>P</em>= 0.004. The higher prevalence of anti-P in patients with lupus nephritis with disappearance during disease remissions supports the hypothesis of an immunopathogenetic role of these antibodies in lupus nephritis. There was also a strong association between anti-dsDNA and anti-P antibodies.</p></div>","PeriodicalId":10683,"journal":{"name":"Clinical immunology and immunopathology","volume":"87 3","pages":"Pages 292-296"},"PeriodicalIF":0.0,"publicationDate":"1998-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1006/clin.1998.4541","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"20565399","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 74
RETRACTIONS 撤稿
Clinical immunology and immunopathology Pub Date : 1998-06-01 DOI: 10.1006/clin.1997.4497
{"title":"RETRACTIONS","authors":"","doi":"10.1006/clin.1997.4497","DOIUrl":"10.1006/clin.1997.4497","url":null,"abstract":"","PeriodicalId":10683,"journal":{"name":"Clinical immunology and immunopathology","volume":"87 3","pages":"Page 314"},"PeriodicalIF":0.0,"publicationDate":"1998-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1006/clin.1997.4497","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"20576363","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Smokeless Tobacco Extracts Activate Complementin Vitro:A Potential Pathogenic Mechanism for Initiating Inflammation of the Oral Mucosa 无烟烟草提取物激活补体蛋白:引发口腔黏膜炎症的潜在致病机制
Clinical immunology and immunopathology Pub Date : 1998-06-01 DOI: 10.1006/clin.1998.4530
Tunhan Chang, Saurabh Chowdhry, Priya Budhu, Richard R. Kew
{"title":"Smokeless Tobacco Extracts Activate Complementin Vitro:A Potential Pathogenic Mechanism for Initiating Inflammation of the Oral Mucosa","authors":"Tunhan Chang,&nbsp;Saurabh Chowdhry,&nbsp;Priya Budhu,&nbsp;Richard R. Kew","doi":"10.1006/clin.1998.4530","DOIUrl":"10.1006/clin.1998.4530","url":null,"abstract":"<div><p>The use of smokeless tobacco has been linked to an increased incidence of inflammation of the buccal and gingival mucosa. However, the mechanisms by which smokeless tobacco initiates inflammation are not well understood. The complement cascade is a ubiquitous source of proinflammatory molecules and can be activated rapidly by a wide variety of agents. Therefore, the effect of smokeless tobacco on complement was investigated as a potential pathogenic mechanism for triggering inflammation of the oral mucosa. Aqueous extracts of loose leaf chewing tobacco (1S1), dry snuff (1S2), and moist snuff (1S3), added to normal human serum, depleted complement hemolytic activity in a dose-dependent manner. Experiments utilizing sera deficient in one specific complement component indicated that the smokeless tobacco-induced depletion of hemolytic activity was due largely to consumption of C3. Furthermore, assays designed to test the activity of the alternative pathway of complement clearly showed that all three extracts depleted the hemolytic activity of this pathway. Finally, all three smokeless tobacco extracts activated the alternative pathway since significantly elevated levels of the cleavage fragments iC3b and Bb were detected in extract-treated serum. High quantities of the classical pathway cleavage fragment C4d also were detected in serum treated with moist snuff (1S3). The results clearly demonstrate that smokeless tobacco extracts activate the alternative pathway and also suggest some measure of classical pathway activation. Activation of complement by smokeless tobacco may be a mechanism for initiating inflammation of the oral mucosa.</p></div>","PeriodicalId":10683,"journal":{"name":"Clinical immunology and immunopathology","volume":"87 3","pages":"Pages 223-229"},"PeriodicalIF":0.0,"publicationDate":"1998-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1006/clin.1998.4530","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"20564838","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 7
Silicone Gel and Animal Models of Autoimmune Disease 有机硅凝胶与自身免疫性疾病的动物模型
Clinical immunology and immunopathology Pub Date : 1998-06-01 DOI: 10.1006/clin.1998.4567
Kimber L. White Jr.
{"title":"Silicone Gel and Animal Models of Autoimmune Disease","authors":"Kimber L. White Jr.","doi":"10.1006/clin.1998.4567","DOIUrl":"10.1006/clin.1998.4567","url":null,"abstract":"","PeriodicalId":10683,"journal":{"name":"Clinical immunology and immunopathology","volume":"87 3","pages":"Pages 205-206"},"PeriodicalIF":0.0,"publicationDate":"1998-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1006/clin.1998.4567","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"20564835","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 3
Myosin-Reactive Autoantibodies in Rheumatic Carditis and Normal Fetus 风湿性心炎和正常胎儿的肌球蛋白反应性自身抗体
Clinical immunology and immunopathology Pub Date : 1998-05-01 DOI: 10.1006/clin.1998.4531
Xiaobing Wu , Bin Liu , Pieter-Luttig Van der Merwe , Neale Nicola Kalis , Seth M. Berney , David C. Young
{"title":"Myosin-Reactive Autoantibodies in Rheumatic Carditis and Normal Fetus","authors":"Xiaobing Wu ,&nbsp;Bin Liu ,&nbsp;Pieter-Luttig Van der Merwe ,&nbsp;Neale Nicola Kalis ,&nbsp;Seth M. Berney ,&nbsp;David C. Young","doi":"10.1006/clin.1998.4531","DOIUrl":"10.1006/clin.1998.4531","url":null,"abstract":"<div><p>EBV-transformed B cells from a 20-week human fetal spleen and from blood of patients with poststreptococcal rheumatic carditis were studied. Most antibodies from nine fetal and six patient myosin-reactive B cell clones were multireactive (reacting with cardiac myosin,<em>Streptococcus pyogenes,</em>and rat cardiac myocytes) which supports a role for molecular mimicry in stimulation of these autoantibodies. Sequence analysis revealed that fetal and patient anti-myosin repertoires were composed of unrelated clones with diverse V gene usages. Fetal and patient antibodies had reduced V<sub>H</sub>CDR3 length on average and reduced light chain N region addition with a low rate of somatic mutation in the variable region genes, characteristics generally associated with fetal B cells but also with some adult B cells. Five of six myosin-reactive patient clones used V<sub>H</sub>3, whereas only two of nine fetal clones used V<sub>H</sub>3, suggesting skewing from the average 50–60% V<sub>H</sub>3 gene usage found in randomly selected adult and fetal antibodies.</p></div>","PeriodicalId":10683,"journal":{"name":"Clinical immunology and immunopathology","volume":"87 2","pages":"Pages 184-192"},"PeriodicalIF":0.0,"publicationDate":"1998-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1006/clin.1998.4531","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"20534350","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 17
Inflammatory Potential of C-Reactive Protein Complexes Compared to Immune Complexes 与免疫复合物相比,c反应蛋白复合物的炎症潜能
Clinical immunology and immunopathology Pub Date : 1998-05-01 DOI: 10.1006/clin.1997.4516
Ivan R. Romero , Carol Morris , Monica Rodriguez , Terry W. Du Clos , Carolyn Mold
{"title":"Inflammatory Potential of C-Reactive Protein Complexes Compared to Immune Complexes","authors":"Ivan R. Romero ,&nbsp;Carol Morris ,&nbsp;Monica Rodriguez ,&nbsp;Terry W. Du Clos ,&nbsp;Carolyn Mold","doi":"10.1006/clin.1997.4516","DOIUrl":"10.1006/clin.1997.4516","url":null,"abstract":"<div><p>C-reactive protein (CRP) is an acute phase serum protein that binds to phosphocholine (PC) and to components of damaged tissue. CRP resembles antibody in that it binds to ligands and activates the classical complement pathway. To compare the processing of CRP complexes to that of IgG complexes, we have prepared complexes containing the same ligand, PC-conjugated BSA, and IgG antibody to either BSA or CRP. We previously demonstrated similar complement-mediated binding of these complexes to erythrocyte complement receptors. CRP and IgG also bind to receptors on neutrophils (PMN), providing another possible pathway for clearance of ligands. PMN binding of IgG complexes can lead to activation with damaging inflammatory consequences. In the present report we have used CRP and IgG complexes containing PC-BSA to compare binding to PMN and activation of PMN adherence to endothelial cells. The results indicate that CRP complexes do not activate PMN whereas IgG complexes do. Binding assays indicate that there is substantially greater binding of IgG than CRP complexes to PMN.</p></div>","PeriodicalId":10683,"journal":{"name":"Clinical immunology and immunopathology","volume":"87 2","pages":"Pages 155-162"},"PeriodicalIF":0.0,"publicationDate":"1998-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1006/clin.1997.4516","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"20534390","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 15
The Role of TGFβ in the Pathogenesis of Human Tuberculosis TGFβ在人结核发病机制中的作用
Clinical immunology and immunopathology Pub Date : 1998-05-01 DOI: 10.1006/clin.1998.4528
Zahra Toossi , Jerrold J. Ellner
{"title":"The Role of TGFβ in the Pathogenesis of Human Tuberculosis","authors":"Zahra Toossi ,&nbsp;Jerrold J. Ellner","doi":"10.1006/clin.1998.4528","DOIUrl":"10.1006/clin.1998.4528","url":null,"abstract":"","PeriodicalId":10683,"journal":{"name":"Clinical immunology and immunopathology","volume":"87 2","pages":"Pages 107-114"},"PeriodicalIF":0.0,"publicationDate":"1998-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1006/clin.1998.4528","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"20534384","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 94
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