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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
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2001
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vol. 49
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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

Cytokines in reumatoid arthritis

100%
Robak T., Gladalska A.
Postępy Higieny i Medycyny Doświadczalnej
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1997
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vol. 51
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issue 6
621-636
EN
In this review we have examined the role of a variety cytokines in the pathogenesis of rheumatoid arthritis (RA) and their possible applications in the treatment of this disease. Cytokines are small protein molecules, released by activated cells which function as chemical messengers between cells of the immune, inflammatory and other systems. The studies using isolated cells from RA synovial membranes indicate that the vast majority of known cytokines are found in RA synovial tissue. These include IL-1, TNFa, IL-6, IL-8, TGFb, GM-CSF and others. TNFa and IL-1 are important 'pivotal' molecules in the disease process. TNFa has been detected in the serum and synovial fluid of patients with RA, sugesting an important contribution of this cytokine to the development of arthritis. Clinically, TNF-a has been also associated with markers of rheumatoid disease activity. Rheumatoid synovial tissue synthesizes large amounts of both forms of IL-1 (IL-1a and IL-1b) in vitro. IL-1 can exert a variety of systemic effects, including induction of fever and synthesis of acute phase proteins. It also induces local joint effects mediating production of fibroblast fibronectin and tissue collagenase. IL-6 is found in greater quantities in the synovial fluids from patients with RA compared to osteoarthritis. Synovial fluid IL-6 levels correlate with local IgM rheumatoid factor and systemic acute phase protein production. Chemokines, including IL-8, have potent chemotactic activity for cells of the immune system. IL-8 not only participates in the inflammatory phase of RA, but also participates in the vasculoproliferative phase of this disease. Recent data on the cytokine profile in RA implies that alternative treatment strategies should be considered. Potential approaches for modifying the cytokine network include inhibition of cytokine production or their action, inhibition of signal transduction and administration of suppressive cytokines.
3

Clinical and genetic heterogeneity of rheumatoid arthritis

100%
Klimiuk P. A., Weyand C. M., Sierakowski S., Goronzy J. J.
Postępy Higieny i Medycyny Doświadczalnej
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2000
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vol. 54
|
issue 6
845-853
EN
The diagnostic category of rheumatoid arthritis, a syndrome of chronic inflammatory disease of the synovial membrane and of extraarticular tissues, covers a broad spectrum of clinical phenotypes. Here we propose that distinct combinations of disease risk genes produce heterogeneity of rheumatoid disease. Recognition of this genetic and clinical heterogeneity has immediate implications as it provides the opportunity to develop selective therapies for the different variants of disease.
4

The role of angiogenesis in rheumatoid arthritis

100%
Pa?gan K.
Postępy Higieny i Medycyny Doświadczalnej
|
2000
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vol. 54
|
issue 6
855-865
EN
The paper presents recent data on the angiogenesis and the angiogenic and angiostatic mediators in rheumatoid arthritis
5

Macrophage migration inhibitory factor and its role in autoimmune diseases

80%
Denkinger C. M., Metz C., Fingerle-Rowson G., Denkinger M. D., Forsthuber T.
Archivum Immunologiae et Therapiae Experimentalis
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2004
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vol. 52
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issue 6
389-400
EN
After several decades of research into the macrophage migration inhibitory factor (MIF), its diverse actions in the immune system are yet to be fully revealed. What has become clear is that MIF plays an important role in both innate and adaptive immunity. However, while several pathways mediating the function of MIF in the immune system have been established, its role in pathogenic states such as autoimmune diseases has remained unresolved. MIF has been implicated in different autoimmune diseases, including rheumatoid arthritis, glomerulonephritis, and multiple sclerosis, but knowledge about the underlying cellular and molecular mechanisms is just emerging. However, overall it appears that the inhibition of its proinflammatory action is likely to be a successful new therapeutic strategy for some autoimmune diseases, possibly by reducing the need for steroids. As more aspects of the role of this cytokine in the pathogenesis of autoimmune diseases are elucidated, better strategies to target it therapeutically can be expected.
6

Cytokines, receptors and inhibitors.Evaluation of their role in laboratory diagnostics of rheumatiod arthritis

80%
Dobryszycka W., Rekas A.
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vol. 47
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issue 6
415-436
7

Genetic polymorphisms of the DNA repair gene MPG may be associated with susceptibility to rheumatoid arthritis

80%
Chen S. Y., Wan L., Huang C. M., Huang Y. C., Sheu J. J. C., Lin Y. J., Liu S. P., Lan Y. C., Lai C. H., Lin C. W., Tsai C. H., Tsai F. J.
Journal of Applied Genetics
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2010
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vol. 51
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issue 4
519-521
EN
Rheumatoid arthritis (RA) is a chronic autoimmune disease and can lead to deformities and severe disabilities, due to irreversible damage of tendons, joints, and bones. A previous study indicated that a DNA repair system was involved in the development of RA. In this study, we investigated the association of four N-methylpurine-DNA glycosylase (MPG) gene polymorphisms (rs3176364, rs710079, rs2858056, and rs2541632) with susceptibility to RA in 384 Taiwanese individuals (192 RA patients and 192 control subjects). Our data show a statistically significant difference in genotype frequency distributions at rs710079 and rs2858056 SNPs between RA patients and control groups (P = 0.040 and 0.029, respectively). Our data also indicated that individuals with the GG genotype at rs2858056 SNP may have a higher risk of developing RA. In addition, compared with the haplotype frequencies between case and control groups, individuals with the GCGC haplotype appeared to be at a greater risk of RA progression (P = 0.003, OR = 1.75; 95% CI = 1.20-1.55). Our results suggest that rs710079 and rs2858056 polymorphisms and the GCGC haplotype in the MPG gene are associated with the risk of RA progression, and thus may be used as molecular markers of RA if they are confirmed by further research.
8

Human sera with precipitating antibodies to human soluble immune complexes. A brief communication

80%
Milgrom F., Czechowski D.
Archivum Immunologiae et Therapiae Experimentalis
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2004
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vol. 52
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issue 3
197-200
EN
Previous numerous papers by the senior author dealt with the human serum factor referred to as anti-antibody which is specifically directed against IgG antibodies that underwent molecular transformation in the course of the reactions with their corresponding antigens. The reactions of this serum factor could be conveniently detected by means of agglutination of Rh-positive erythrocytes sensitized by anti Rh antibodies. No precipitation tests could be developed.Most studies were conducted by means of double diffusion in gel precipitation. Most studies were conducted by means of double diffusion in gel precipitation.Sera with precipitating anti-antibodies may serve as exquisite reagents for detection of soluble immune complexes in human sera.
9

Neuro-endocrine-immune axis in human rheumatoid arthritis

80%
Sakane T., Suzuki N.
Archivum Immunologiae et Therapiae Experimentalis
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2000
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vol. 48
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issue 5
417-428
EN
We present an overview of the role of neuro-endocrine-immune mechanisms in the pathophysilogical responses of patients with rheumatoid arthritis (RA). In patients with RA proinflammatory cytokines secreted by synovial cells provoke local inflammation in the joints and, simultaneously, initiate a systemic acute phase response. Thus, profund changes of the neuro-endocrine-immune axis could take place in the patients. Defects in the hypothalamus-pituitary-adrenal axis have been observed in patients with RA. Prolactin levels are often elevated and a abnormal sex hormone levels have been described in RA patients. Defective neural regulation of inflammation involving neuropeptides at least partly plays a pathogenic role in RA.We and others have found that participants of the neuro-endocrine-immune interactions, such as hormones, neurotransmitters and neuropeptides, modulate RA synovial cell functions and that they are actually produced by, and their receptors are expressed on, cells within the inflammatory joint compartment. Thus, neuropeptides and hormones not only affect a systemic acute phase response of RA patients, but also modulate local inflammation directly in RA joints. These results suggest that defects in regulatory processes, which are fundamental to RA, may lie in the immune system, the nervous system, the endocrine system or the interactions of these. A better understanding of neuro-endocrine-immune interactions holds the promise of new approaches to the treatment of RA with the use of hormones, neurotransmitters, neuropeptides and/or their antagonists.
10

T cell chemokine receptor expression in human Th1- and Th2-associated diseases

61%
Campbell J. D., Hayglass K. T.
Archivum Immunologiae et Therapiae Experimentalis
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2000
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vol. 48
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issue 5
451-456
EN
The interaction between chemokines and their receptors is an important step in the control of leukocyte migration into sites of inflammation. Chemokines also mediate a variety of effects independent of chemotaxis, including induction and enhancement of Th1- and Th2---associated cytokine responses. Recent studies have shown that human Th1 and Th2 clones, activated under polarizing conditions with polyclonal stimuli in vitro, display distinct patterns of chemokine receptor expression: Th1 clones preferentially express CCR5 and CXCR3 while many Th2 clones express CCR4, CCR8 and, to a lesser extent, CCR3. These differential patterns of chemokine receptor expression suggest a mechanism for selective induction of migration and activation of Th1- and Th2-type cells during inflammation and, perhaps, normal immune homoeostasis. Studies have begun to examine T cell chemokine receptor expression in vivo to determine the relevance of these in vitro observations to human Th1 and Th2-associated diseases. In this review, we critically examine recent reports of T cell chemokine receptor expression in human autoimmune disorders (multiple sclerosis and rheumatoid arthritis) and atopic disorders (allergic rhinitis and asthma) which are believed to arise from inappropriate Th1- and Th2-dominated responses, respectively.
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