Full-text resources of PSJD and other databases are now available in the new Library of Science.
Visit https://bibliotekanauki.pl
Preferences help
Polish version English version Language
enabled [disable] Abstract
Number of results

Results found: 6

Number of results on page
first rewind previous Page / 1 next fast forward last

Search results

Search:
in the keywords:  AUTOANTIBODY
help Sort By:

help Limit search:
first rewind previous Page / 1 next fast forward last
1

Serum autoantibodies profile and increased levels of circulating intercellular adhesion molecule-1: a reflection of the immunologically mediated systemic vasculopathy in rheumatic diseases?

100%
Kuryliszyn-Moskal A., Klimiuk P. A., Sierakowski S.
Archivum Immunologiae et Therapiae Experimentalis
|
2001
|
vol. 49
|
issue 6
423-430
EN
Clinical manifestation of systemic vasculitis may be postulated as a consequence of the immune response abnormalities in the course of connective tissue diseases (CTD). The aim of this study was to elucidate the significance of the different autoantibodies and soluble intercellular adhesion molecule 1 (sICAM-1) shedding into the circulation in the diagnosis of vasculitis in rheumatic diseases. Serum of 86 patients with rheumatic diseases (54 with rheumatoid arthritis (RA) and 32 with CTD) were analyzed for the concentrations of sICAM-1 levels by the enzyme linked immunosorbent assay (ELISA). Control sera were obtained from 30 healthy individuals. Anti-nuclear antibodies (ANA), anti-double-stranded antibodies (anti-dsDNA) and anti-proteinase-3 (PR-3) antibodies (anti-neutrophil cytoplasmic autoantibodies cytoplasmic specific, cANCA) were assessed by the ELISA method. Fifty out of 86 patients had the systemic lesions. Pathological picture of the vascular loop in the nailfold capillary microscopy was found in 84 patients. In 19 patients the microvascular changes were advanced, in 35 moderate and in 30 mild. All patients with the articular manifestations had the pathological changes in the capillary microscopy. Patients with advanced changes in the capillary microscopy had the longer disease duration compared to patients with mild intensity of vasculitis. Serum concentration of sICAM-1 was significantly increased in RA and CTD patients compared to 30 controls (in both cases p<0.001). Moreover, RA and CTD patients with the systemic vasculitis showed significantly higher levels of sICAM-1 than those without vascular involvement (respectively p<0.001 and p<0.005). ANA were observed in significantly elevated concentration among RA and CTD patients with the systemic damage compare to patients without organ injury (respectively p<0.001 and p<0.05). Also cANCA level was twice more higher but only among CTD patients with the systemic damage (p<0.05). Serum concentration of sICAM-1 was elevated in studied patients with the presence of ANA antibodies (p<0.05). Significant correlation between ANA level and the disease duration, and hemoglobin concentration were observed. The concentration of cANCA correlated with rheumatoid factor and of dsDNA with patient age. We conclude that the systemic lesions in the course of RA and CTD are accompanied by the microvascular injury in nailfold capillary microscopy. Our data suggest that sICAM-1, ANA and cANCA serum levels may reflect the extent of the vascular involvement in RA and CTD patients.
2

Systemic lupus erythematosus ? recent clues from congenic strains

80%
Henry T., Mohan C.
Archivum Immunologiae et Therapiae Experimentalis
|
2005
|
vol. 53
|
issue 3
207-212
EN
Systemic lupus erythematosus is a polycongenic autoimmune disease characterized by the production of antinuclear antibodies that lead to subsequent end organ damage. The study of lupus is complicated by its polycongenic origin, contributions from hormones and the environment, epistasis among susceptibility loci, suppressive modifiers, and the fact that a single susceptibility locus may encompass multiple susceptibility genes. Murine models that develop lupus spontaneously have greatly contributed to our understanding of this disease. In particular, the advent of ?congenic strains' has greatly simplified the study of this complex autoimmune disease. Thus, congenic strains bearing NZB/NZW/NZM2410, BXSB, and MRL lupus susceptibility loci are steadily replacing the traditionally studied murine lupus models as the models of choice for research. This review summarizes how researchers have used congenic strains over the past few years to dissect out and reconstruct the individual elements contributing to lupus pathogenesis.
3

Anti-GBM glomerulonephritis: a T cell-mediated autoimmune disease?

80%
Lou Y.-H.
Archivum Immunologiae et Therapiae Experimentalis
|
2004
|
vol. 52
|
issue 2
96-103
EN
Anti-glomerular basement membrane (GBM) glomerulonephritis, which was among the earliest recognized human autoimmune diseases, is characterized by the presence of anti- -GBM antibody. It has been a prototypical example of autoantibody-mediated autoimmune disease. However, decades of research on this disease, based either on clinical observations or experimental models, have revealed that T cell-mediated cellular immunity may potentially be a more important mediator of glomerulonephritis. We have made several breakthroughs in understanding the T cell-mediated mechanism causing this disease in a rat model based on Goodpasture's antigen, non-collagen domain 1 of ?3 chain of type IV collagen (Col4alpha3NC1). We demonstrated that anti-GBM glomerulonephritis was induced by either passive transfer of Col4alpah3NC1-specific T cells or active immunization with the nephritogenic T cell epitope of Col4alpha3NC1. Immunization with the T cell epitope also triggered production of anti-GBM antibodies to diversified GBM antigens. Thus, a single nephritogenic T cell epitope alone is sufficient to induce the clinical spectrum of anti-GBM glomerulonephritis, including proteinuria, glomerular injury, and anti-GBM antibody. A possible T cell-mediated mechanism for causing human anti-GBM disease is proposed.
4

Experimental anti-GBM nephritis as an analytical tool for studying spontaneous lupus nephritis

80%
Du Y., Fu Y., Mohan C.
Archivum Immunologiae et Therapiae Experimentalis
|
2008
|
vol. 56
|
issue 1
31-40
EN
Systemic lupus erythematosus (SLE) is an autoimmune disease that results in immune-mediated damage to multiple organs. Among these, kidney involvement is the most common and fatal. Spontaneous lupus nephritis (SLN) in mouse models has provided valuable insights into the underlying mechanisms of human lupus nephritis. However, SLN in mouse models takes 6?12 months to manifest; hence there is clearly the need for a mouse model that can be used to unveil the pathogenic processes that lead to immune nephritis over a shorter time frame. In this article more than 25 different molecules are reviewed that have been studied both in the anti-glomeruali basement membrane (anti-GBM) model and in SLN and it was found that these molecules influence both diseases in a parallel fashion, suggesting that the two disease settings share common molecular mechanisms. Based on these observations, the authors believe the experimental anti-GBM disease model might be one of the best tools currently available for uncovering the downstream molecular mechanisms leading to SLN.
5

Sjogren's syndrome: immunological response underlying the disease

80%
Brayer J. B., Humphreys-Beher M. G., Peck A. B.
Archivum Immunologiae et Therapiae Experimentalis
|
2001
|
vol. 49
|
issue 5
353-360
EN
Sjogren's syndrome is a chronic autoimmnune disorder characterized primarily by the discomforts od dry eyes and dry mouth due to the progressive loss of exocrine gland function. Development of a number of animal models to study Sjogren's syndrome, especially the NOD mouse and its congenic partner strains, has permitted a systematic analysis of immunological and non-immunological factors that influence predisposition for development of the autoimmune response. These data are reviewed here.
6

Deconstructing B cell tolerance to basement membranes

70%
Foster M. H., Zhang Y., Clark A. G.
Archivum Immunologiae et Therapiae Experimentalis
|
2006
|
vol. 54
|
issue 4
227-237
EN
Basement membrane antigens are frequent targets of autoantibody attack in systemic and organ-restricted autoimmunity. These specialized and highly organized matrices are composed of multiple components with restricted tissue distributions and limited epitope exposure. To the dissect mechanisms controlling humoral autoimmunity to nephritogenic basement membrane antigens, we developed autoantibody transgenic models. In mice bearing the LamH Ig transgene encoding B cell receptors specific for laminin, autoreactive B cells are readily generated but actively regulated in vivo. In this model, anti-laminin B cells are immunologically censored by mechanisms that include central deletion, k light-chain editing, and anergy. Tolerance is maintained when the transgene is established in MRL and BXSB genetic backgrounds with inherited autoimmune susceptibility, and despite provocation with potent environmental stimulants. Collectively, these studies indicate that the pathogenic anti-laminin reactivity characteristic of systemic lupus is tightly regulated. A novel anti-collagen transgenic model is used to assess the tolerogenesis of a structurally distinct pathogenic basement membrane epitope and to determine if the reactivity to putative cryptic epitopes targeted in organ-restricted disease is regulated. These studies should provide insight into the molecular mechanisms controlling basement membrane autoreactivity and ultimately facilitate the development of novel strategies to inactivate autoreactive cells and treat autoimmune disease.
first rewind previous Page / 1 next fast forward last
JavaScript is turned off in your web browser. Turn it on to take full advantage of this site, then refresh the page.