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  • 1
    Electronic Resource
    Electronic Resource
    Circulating Immune Complexes and Complement C4 Null Alleles in Patients Operated on for Premature Atherosclerotic Peripheral Vascular Disease (1999)
    Springer
    Journal of clinical immunology 19 (1999), S. 406-413 
    Details
    ISSN: 1573-2592
    Keywords: Circulating immune complexes ; complement factor C4 deficiency ; peripheral atherosclerosis ; premature atherosclerosis
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Circulating immune complexes can lead to vascular inflammation and premature atherosclerosis and the fourth component of complement, C4, plays an important role in the removal of immune complexes. The objective of this study was to analyze the relation between circulating immune complexes and C4 null alleles in patients operated on for peripheral vascular disease before the age of 50. The prevalence of circulating immune complexes and null alleles of C4 (C4Q0) was determined in 62 patients with peripheral atherosclerosis requiring surgery before 50 years of age and in a matched control group. C4A and C4B null alleles (C4A*Q0, C4B*Q0) were determined by electrophoresis of plasma, followed by immunofixation. C4A and C4B concentrations were measured by ELISA. Circulating immune complexes were determined by sucrose density gradient centrifugation and gel filtration. There was no difference in the distribution of C4Q0 between patients and controls. The patients had higher prevalences and levels of circulating immune complexes. This was correlated with the presence of C4Q0, especially C4A*Q0. There was an inverse correlation of concentration of circulating immune complexes with C4A levels and with ratio of C4A/B levels. Thus, a significant proportion of patients with premature peripheral atherosclerosis had circulating immune complexes and C4A*Q0 enhanced the propensity to immune complex formation. This might represent one mechanism for vascular damage in this patient group.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1023/A:1020506901117
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  • 2
    Electronic Resource
    Electronic Resource
    Expanded T Cell Populations in Patients with Wegener's Granulomatosis: Characteristics and Correlates with Disease Activity (1998)
    Springer
    Journal of clinical immunology 18 (1998), S. 404-413 
    Details
    ISSN: 1573-2592
    Keywords: T cell receptor ; expanded T cells ; phenotypic markers ; Wegener's granulomatosis ; cytokines
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Patients with Wegener's granulomatosis have a high prevalence of expanded populations of CD4+ and CD8+ T cells bearing different α/β T cell receptors. To elucidate the role of these populations, we studied the phenotypic and functional characteristics of 13 expanded T cell populations in four patients for a period of 35–51 months. The expanded populations generally showed a persistently high expression of the activation markers HLA-DR and CD25. This expression was independent of the activity of the disease. The expanded populations also expressed CD45RO and/or CD45RA and most of them expressed CD57 but not CD28. Analysis of intracellular presence and secretion of IFN-γ, IL-2, and IL-4 showed that most of the expanded cell populations contained and/or secreted more of these cytokines than the nonexpanded populations, with an especially high expression/secretion of IFN-γ and IL-2. The expanded populations showed little proliferative response to Con A and OKT3. The proliferative response of the cells was partly restored after preincubation in medium alone. Some of the expanded populations were associated with disease activity, thus suggesting a link between expanded T cells and the disease. The activated status of the expanded populations and the tendency for certain populations to correlate in magnitude with disease activity suggest their involvement in the disease process. The relative stability of these cell populations indicates that the stimulus driving them is persistent, in agreement with the chronicity of the disease.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1023/A:1023230722874
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    Paper (German National Licenses)
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  • 3
    Electronic Resource
    Electronic Resource
    Cellular immune response of patients with uveitis to peptide M, a retinal S-antigen fragment (1993)
    Springer
    Journal of clinical immunology 13 (1993), S. 352-358 
    Details
    ISSN: 1573-2592
    Keywords: Lymphocyte proliferation assay ; peptide M ; yeast histone H3 ; retinal S-antigen ; uveitis
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Peptide M, an 18-amino acid fragment from position 303 to position 320 of retinal S-antigen, produces experimental autoimmune uveitis (EAU), similar to that produced by native S-antigen, in several vertebrate species including nonhuman primates. It was observed that 12 of the 39 (30.7%) patients with uveitis, 1 of the 29 (3.4%) patients with systemic connective tissue disorders (CTD) without eye involvement, 2 of the 7 (5.8%) patients of CTD with uveitis, 1 of the 17 (5.8%) patients with diabetic retinopathy, and none of the 19 normal healthy controls showed a significant lymphoproliferative response to peptide M (stimulation index of 3 or more). Yeast histone H3 peptide gave a positive response in 1 (2.5%), 2 (6.8%), 1 (14.2%), 2 (11.7%), and 2 (10.5%) individuals, respectively, in the different groups studied. In a few cases a positive response to yeast histone H3 peptide was observed without significant stimulation to peptide M. These findings indicate that peptide M could also be an immunogenic epitope of S-antigen in humans and be aetiopathologically related to uveitis in a subset of patients with this disease. However, unlike experimental animals, the responses to peptide M and yeast histone H3 were nonconcordant, necessitating further studies.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00920244
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    Paper (German National Licenses)
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