Experimental and clinical immunogenetics最新文献_第9页

The human immunoglobulin heavy diversity (IGHD) and joining (IGHJ) segments. 人免疫球蛋白重多样性(IGHD)和连接(IGHJ)段。

Experimental and clinical immunogenetics Pub Date : 1999-01-01 DOI: 10.1159/000019109

M Ruiz, N Pallarès, V Contet, V Barbi, M P Lefranc

引用次数: 58

Multiple sclerosis: association to HLA DQalpha in a tropical population. 多发性硬化症:与热带人群HLA dqα的关系。

Experimental and clinical immunogenetics Pub Date : 1999-01-01 DOI: 10.1159/000019105

M Arcos-Burgos, G Palacio, J L Sánchez, A C Londoño, C S Uribe, M Jiménez, A Villa, J M Anaya, M L Bravo, N Jaramillo, C Espinal, J J Builes, M Moreno, I Jiménez

{"title":"Multiple sclerosis: association to HLA DQalpha in a tropical population.","authors":"M Arcos-Burgos, G Palacio, J L Sánchez, A C Londoño, C S Uribe, M Jiménez, A Villa, J M Anaya, M L Bravo, N Jaramillo, C Espinal, J J Builes, M Moreno, I Jiménez","doi":"10.1159/000019105","DOIUrl":"https://doi.org/10.1159/000019105","url":null,"abstract":"Studies performed in subtropical populations have found significant association between the phenotype multiple sclerosis (MS) and the major histocompatibility complex (MHC). We present the results of a case-control study conducted on a tropical population (Antioquia, Colombia) in order to detect a possible association between MS and HLA DQalpha (HLA DQA1*) alleles. Forty chromosomes belonging to MS patients were compared to two sets of controls (40 and 910 chromosomes, respectively). The HLA DQA1*0101 and DQA1*0102 alleles were found in a significantly higher proportion among the cases than among the controls, whereas the HLA DQA1*0103 allele was found in a significantly lower proportion of the cases. These results suggest that the association of HLA DQA1*0101, DQA1*0102 and DQA1*0103 to the MS phenotype found in Caucasian subtropical populations remains in individuals with MS inhabiting the tropics. This finding could mean that the major genetic component associated to the MHC in subtropical populations is the same in the tropics.","PeriodicalId":77124,"journal":{"name":"Experimental and clinical immunogenetics","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"1999-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1159/000019105","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"21261575","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

Analysis of two IL-4 promoter polymorphisms in a cohort of atopic and asthmatic subjects. 一组特应性和哮喘患者IL-4启动子多态性分析。

Experimental and clinical immunogenetics Pub Date : 1999-01-01 DOI: 10.1159/000019094

S Hook, P Cheng, J Holloway, G Riley, G Sawyer, G Le Gros, R Beasley

引用次数: 11

Genetic polymorphism of human complement factor I (C3b inactivator) in the Chinese Han population. 中国汉族人群补体因子I (C3b失活因子)基因多态性

Experimental and clinical immunogenetics Pub Date : 1999-01-01 DOI: 10.1159/000019093

L Zhang, B Stradmann-Bellinghausen, C Rittner, P M Schneider

引用次数: 2

No quantitative relationship between CR1 and Lutheran expression on erythrocytes: In(Lu) gene product is not a common regulator of CR1 expression on erythrocytes. CR1与Lutheran在红细胞中的表达无定量关系:In(Lu)基因产物不是红细胞中CR1表达的常见调节因子。

Experimental and clinical immunogenetics Pub Date : 1999-01-01 DOI: 10.1159/000019098

S Oudin, P Y Lepennec, X Dervillez, M Tonye-Libyh, T Tabary, F Philbert, F Bougy, B Reveil, J L Pennaforte, P Rouger, J H Cohen

{"title":"No quantitative relationship between CR1 and Lutheran expression on erythrocytes: In(Lu) gene product is not a common regulator of CR1 expression on erythrocytes.","authors":"S Oudin, P Y Lepennec, X Dervillez, M Tonye-Libyh, T Tabary, F Philbert, F Bougy, B Reveil, J L Pennaforte, P Rouger, J H Cohen","doi":"10.1159/000019098","DOIUrl":"https://doi.org/10.1159/000019098","url":null,"abstract":"The density of CR1, the C3b/C4b receptor (CD35), on erythrocytes (E) (CR1/E) is genetically determined. However, the broad distribution of CR1/E within a given genotype suggests that other genetic elements might contribute to the regulation of CR1/E. In some pathological conditions, including systemic lupus erythematosus (SLE), AIDS and hemolytic anemia, CR1 deficiency parallels the severity of the disease. When compared to healthy individuals, an accelerated decrease in CR1/E in these patients has been demonstrated, but other mechanisms interfering with CR1 density regulation during erythropoiesis might also contribute. In exceptional circumstances, CR1/E can be dramatically decreased in healthy individuals by the effect of a regulatory gene, In(Lu), that switches off various surface molecules on E, the structure genes of which are located on four different chromosomes, suggesting a transcription regulatory role for In(Lu) gene products. The hypothesis that products of this gene could physiologically regulate the surface density of all these molecules has been tested by determining Lub density on E (Lub/E) using quantitative flow cytometry. Lub antigenic sites were then compared to CR1/E among healthy individuals of the different CR1 density phenotypes, SLE patients with and without CR1 deficiency, and an exceptional SLE patient totally lacking CR1/E and reticulocytes. No quantitative relationship was found between CR1 and Lub expression in either normal or pathological conditions. These data establish that In(Lu) products are not involved in normal or pathological CR1 density regulation.","PeriodicalId":77124,"journal":{"name":"Experimental and clinical immunogenetics","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"1999-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1159/000019098","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"21212634","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: 2

An unequal crossover between the RCCX modules of the human MHC leading to the presence of a CYP21B gene and a tenascin TNXB/TNXA-RP2 recombinant between C4A and C4B genes in a patient with juvenile rheumatoid arthritis. 人MHC的RCCX模块之间的不平等交叉导致C4A和C4B基因之间存在CYP21B基因和tenascin TNXB/TNXA-RP2重组。

Experimental and clinical immunogenetics Pub Date : 1999-01-01 DOI: 10.1159/000019099

K L Rupert, R M Rennebohm, C Y Yu

{"title":"An unequal crossover between the RCCX modules of the human MHC leading to the presence of a CYP21B gene and a tenascin TNXB/TNXA-RP2 recombinant between C4A and C4B genes in a patient with juvenile rheumatoid arthritis.","authors":"K L Rupert, R M Rennebohm, C Y Yu","doi":"10.1159/000019099","DOIUrl":"https://doi.org/10.1159/000019099","url":null,"abstract":"The RCCX module of the human MHC class III region is comprised of four genes arranged in tandem: RP, complement C4, steroid 21-hydroxylase (CYP21), and tenascin X (TNX). Variations in the number and genes of the RCCX modules may lead to genetic and/or autoimmune diseases. Restriction fragment length polymorphism (RFLP) analysis was utilized to determine the RCCX modular variation in patients with juvenile rheumatoid arthritis (JRA). In JRA patient L1, RFLP analysis suggested the presence of a bimodular RCCX structure containing both C4A long and C4B short genes, yet missing the markers for the CYP21A and TNXA genes usually located between the C4A and C4B genes. The 7.5-kb genomic fragment spanning the CYP21-TNX-RP2 genes was cloned and sequenced, revealing that a genetic recombination occurred between TNXA of a bimodular RCCX chromosome and TNXB of a monomodular RCCX chromosome. This recombination results in a new MHC haplotype with a CYP21B gene and a TNXB/TNXA-RP2 recombinant between the two C4 genes. Elucidation of the breakpoint region provides further evidence for the instability of the MHC class III gene region as a result of the RCCX modular variation.","PeriodicalId":77124,"journal":{"name":"Experimental and clinical immunogenetics","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"1999-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1159/000019099","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"21212635","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: 38

Analysis of immunoglobulin VH and TCR cbeta polymorphisms in a large family with thyroid autoimmune disorder. 甲状腺自身免疫性疾病大家族免疫球蛋白VH和TCR cbeta多态性分析

Experimental and clinical immunogenetics Pub Date : 1999-01-01 DOI: 10.1159/000019110

F Fakhfakh, A Maalej, H Makni, M Abid, J Jouida, M Zouali, H Ayadi

引用次数: 15

Modulation of C5a-mediated effector functions of human polymorphonuclear leukocytes by tumor necrosis factor alpha and granulocyte macrophage colony-stimulating factor. 肿瘤坏死因子α和粒细胞巨噬细胞集落刺激因子对c5a介导的人多形核白细胞效应功能的调节。

Experimental and clinical immunogenetics Pub Date : 1999-01-01 DOI: 10.1159/000019113

R Binder, A Kress, M Kirschfink

{"title":"Modulation of C5a-mediated effector functions of human polymorphonuclear leukocytes by tumor necrosis factor alpha and granulocyte macrophage colony-stimulating factor.","authors":"R Binder, A Kress, M Kirschfink","doi":"10.1159/000019113","DOIUrl":"https://doi.org/10.1159/000019113","url":null,"abstract":"At the site of acute inflammation, leukocytes are confronted with multiple mediators which are expected to modulate each other with respect to cell responses to the individual ligand. In the present study, we compared the effects of the classical chemoattractants FMLP, PAF and LTB4, of the chemokine IL-8 and of TNFalpha, GM-CSF, IFN-gamma and IL-1beta on C5a-induced chemotaxis, degranulation, oxidative burst and expression of adhesion molecules of human neutrophils in vitro. Upon preincubation, TNFalpha as well as GM-CSF dose-dependently inhibited C5a-mediated chemotaxis, but augmented the release of elastase as well as respiratory burst activity. The effects of the two cytokines were accompanied by a downregulation of C5a receptors as determined by Scatchard analysis using (125)I-labeled C5a. Compared on a molar basis, TNFalpha was more effective than GM-CSF. C5a-induced expression of beta(2)-integrins was only moderately influenced by TNFalpha and GM-CSF. C5a itself diminished chemotaxis as well as degranulation and oxidative burst in response to a second dose of the same ligand (homologous desensitization), whereas heterologous desensitization by FMLP and IL-8 was restricted to C5a-induced degranulation or not observed (PAF, LTB4]. The cytokine effects are likely to be a consequence of altered C5a receptor expression as well as of postreceptor events. In concert with C5a, certain cytokines may shift neutrophil effector functions from migration to exocytosis, an essential step within the sequence of events in a coordinated inflammatory response.","PeriodicalId":77124,"journal":{"name":"Experimental and clinical immunogenetics","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"1999-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1159/000019113","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"21433833","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: 21

Interleukin-15 enhances HIV-1-driven polyclonal B-cell response in vitro. 白细胞介素-15增强体外hiv -1驱动的多克隆b细胞应答

Experimental and clinical immunogenetics Pub Date : 1999-01-01 DOI: 10.1159/000019108

L Kacani, G M Sprinzl, A Erdei, M P Dierich

{"title":"Interleukin-15 enhances HIV-1-driven polyclonal B-cell response in vitro.","authors":"L Kacani, G M Sprinzl, A Erdei, M P Dierich","doi":"10.1159/000019108","DOIUrl":"https://doi.org/10.1159/000019108","url":null,"abstract":"Interleukin-15 (IL-15) is a recently described cytokine, produced by monocytes/macrophages, with biological activities similar to IL-2. Since IL-15 was shown to stimulate human B-cell proliferation and immunoglobulin secretion, we investigated its effect on human B-cells stimulated with heat-inactivated human immunodeficiency virus type 1 (iHIV-1) in vitro. We observed a dose-dependent elevation of [3H]-thymidine incorporation and immunoglobulin production by B-cells incubated in the presence of iHIV-1. Moreover, IL-15 stimulated HIV-1-driven B-cell proliferation similarly to IL-2. As to immunoglobulin secretion, IL-15 was able to potentiate the stimulatory effect of IL-10. The highest amounts of iHIV caused a decrease in B-cell proliferation and immunoglobulin secretion to baseline levels, even in the presence of cytokines. These findings indicate that during the late stages of AIDS, when monocytes/macrophages become the major site of viral production, IL-15, in concert with other monocyte-derived cytokines, may promote polyclonal B-cell activation and hypergammaglobulinaemia, which are frequently associated with HIV infection.","PeriodicalId":77124,"journal":{"name":"Experimental and clinical immunogenetics","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"1999-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1159/000019108","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"21261578","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: 33

Plasma alpha1,3-fucosyltransferase deficiency in schizophrenia. 精神分裂症患者血浆α 1,3-聚焦转移酶缺乏。

Experimental and clinical immunogenetics Pub Date : 1999-01-01 DOI: 10.1159/000019104

S Yazawa, S Tanaka, T Nishimura, K Miyanaga, N Kochibe

引用次数: 11