Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P01889 (ankylosing spondylitis)
 5,717 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

To investigate the source of increased production causing elevation of serum immunoglobulin A (IgA) in ankylosing spondylitis (AS) we studied the production of IgA and IgA subclasses in cultures of bone marrow cells as well as the relative numbers of IgA and IgA subclass containing bone marrow cells obtained from 24 patients with AS and 22 healthy control individuals. In patients with AS serum levels of IgA, IgA, and IgA2 were significantly higher compared to controls. The IgA1 subclass in patient's serum contributed significantly less to the total IgA compared to controls. In bone marrow cultures of patients with AS and controls the production of IgA, IgA1 and IgA2 were in the same range as were the relative numbers of bone marrow cells containing IgA and IgA subclasses. However, the immunoglobulin synthesis by bone marrow cells of patients with AS showed a significant shift towards IgA1 compared to controls. Our findings indicate that the regulatory abnormalities of IgA production in AS involve both the IgA1 and IgA2 subclass and suggest that an abnormal mucosal immune response could be responsible for chronic overproduction of IgA and the elevation of serum IgA in patients with AS.
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PMID:Bone marrow IgA and IgA subclass synthesis in ankylosing spondylitis. 837 Dec 35

The various subsets of serum IgA were determined in 43 patients with ankylosing spondylitis to investigate the putative mucosal origin of increased IgA concentrations in this disease. Total IgA was shown to be increased and weakly correlated with the erythrocyte sedimentation rate (ESR). In contrast, although the mean concentration (but not the median) of secretory IgA (SIgA) was slightly increased, no correlation was found with total IgA nor the ESR. Moreover, molecular sieving of nine serum samples selected for their high concentrations of total IgA, and absorption with insoluble jacalin showed these immunoglobulins to be essentially monomers of the IgA1 subclass. These results are consistent with a non-secretory origin of the increase of serum IgA, which must be ascribed to the central immune system.
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PMID:Increased levels of serum IgA as IgA1 monomers in ankylosing spondylitis. 161 65

Elevated serum levels of IgA, IgA1, and IgA2 rheumatoid factors (RF) were demonstrated by enzyme-linked immunosorbent assay in 69%, 73%, and 36%, respectively, of 100 patients with rheumatoid arthritis (RA), whereas fewer than 5% of 100 healthy donor sera contained elevated levels of these RFs. In serum samples from 125 controls with 4 different chronic diseases (systemic lupus erythematosus, ankylosing spondylitis, bronchial asthma, and polyarteritis nodosa), levels of IgA-, IgA1-, and IgA2-RF were found to be increased in 7%, 7%, and 8%, respectively. Comparison of RF levels in samples of serum, synovial fluid (SF), and saliva from RA patients indicated local production of both IgA-RF subclasses in salivary glands and in synovial tissue. Significant positive correlations were found between levels of IgA-RF subclasses in SF and serum, but not in serum and saliva or in SF and saliva. Fractionation of serum, SF, and saliva from patients with RA (by high performance liquid chromatography under acidic conditions) demonstrated that both IgA subclasses with RF activity occur mainly in fractions that also contain IgM. The results of this study show that 1) IgA-RF in serum and SF is mainly of IgA1 subclass, 2) both IgA-RF subclasses are produced locally in salivary glands and in synovial tissue, 3) the production of both IgA-RF subclasses at mucosal and nonmucosal sites is independent from each other, and 4) both IgA-RF subclasses occur predominantly in polymeric form in serum, SF, and saliva in RA patients.
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PMID:Subclass distribution and size of human IgA rheumatoid factor at mucosal and nonmucosal sites. 205 31

The subclass distribution of IgG and IgA plasma cells, and in IgG and IgA rheumatoid factor (RF) producing cells was studied in sections of synovial tissue from seropositive RA and various types of seronegative arthritis, including ankylosing spondylitis, psoriatic arthritis, and Reiter's syndrome. The study was performed with immunofluorescence technique and monoclonal IgG and IgA subclass specific antibodies. IgG RF producing cells were identified by their ability to bind and activate factors both in the early (C3) and late (C5b-9) part of the complement cascade. IgA RF cells were identified by double staining experiments with heat-aggregated IgG and monoclonal antibodies to IgA subclasses. In 23 tissues tested for total IgG, IgG1 cells were usually predominant, while the frequency of IgG3 cells was usually higher than that of IgG2. In 19 tissues also tested for IgA, both IgA subclasses were present in all tissues. IgA1 plasma cells were always predominant, with a mean ratio of IgA1 to IgA2 cells of approximately 10. In the 13 tissues tested for RF-producing cells, the highest frequency of IgG RF cells was found among the IgG3 cells, followed by IgG1 and IgG2. IgA RF cells were found in only one case, all cells being IgA1.
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PMID:IgG and IgA subclass distribution of total immunoglobulin and rheumatoid factors in rheumatoid tissue plasma cells. 221 30

Immunoglobulin synthesis by peripheral blood lymphocytes and serum IgA subclasses were investigated in patients with ankylosing spondylitis (AS) with and without accompanying microscopic hematuria, and HLA-B27 positive and negative healthy controls. An increase in serum IgA, restricted to subclass IgA1, was found in patients with AS, especially in those with microscopic hematuria. IgA synthesis was not increased, but a significant shift to subclass IgA1 was found. Our results resemble abnormalities previously noted in primary IgA nephropathy, and further support the pathogenetic role of IgA in AS.
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PMID:Immunoglobulin synthesis by peripheral blood lymphocytes in patients with ankylosing spondylitis. 326 40

To obtain insight into the immunoregulatory mechanisms in patients with different rheumatic diseases, the occurrence and the subclass distribution of IgA and IgG antibodies against Clq (anti-ClqAb) was determined. In patients with systemic lupus erythaematosus (SLE) the highest frequency of increased serum levels of IgG anti-ClqAb were found, whereas IgA anti-ClqAb were predominantly present in patients with ankylosing spondylitis (AS) and patients with rheumatoid arthritis complicated by vasculitis (RV). In all the IgA anti-ClqAb positive AS and RV patients the antibody reactivity involved the IgA1 subclass while the IgA2 subclass was found in 47% of the patients. Further characterization of the IgA anti-Clq binding activity in sera of AS patients revealed that both subclasses of IgA anti-ClqAb were predominantly polymeric; the binding of both IgA subclasses with solid phase Clq was inhibitable by aggregated fluid phase Clq; we found no detectable interference of rheumatoid factor in the test system for the measurement of IgA anti-ClqAb. In patients with SLE the IgG anti-ClqAb reactivity was mainly of the IgG2 and IgG3 subclass, whereas in the same patients the IgG anti-tetanus toxoid response was not restricted to these subclasses. The predominance of IgG2 and IgG3 subclass of anti-ClqAb in sera of SLE patients, suggests a skewing of the anti-ClqAb response. The observation that the IgA anti-ClqAb of both subclasses is predominantly polymeric in nature and the notion that polymeric IgA is associated with activation of inflammation cascades, suggests that IgA anti-ClqAb may contribute to tissue damage.
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PMID:Subclass distribution of IgA and IgG antibodies against Clq in patients with rheumatic diseases. 789 27

IgA1 and IgA2 subclass serum antibodies against whole Klebsiella pneumoniae bacteria were studied earlier in the sera of 98 patients with ankylosing spondylitis (AS) and in 100 healthy blood donors by enzyme immunoassay. In this study, the patients were divided into groups according to the clinical picture, i.e., the presence or absence of iritis and enthesitis. The previous findings of increased IgA1 and IgA2 subclass antibody levels against K. pneumoniae in AS patients when compared to the healthy controls were not specifically associated with any single AS patient group in the present study, but instead were similarly seen in all patient groups with/without extra-articular features. This is in line with the previous studies suggesting a role for K. pneumoniae in the pathogenesis of AS.
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PMID:Similarly increased serum IgA1 and IgA2 subclass antibody levels against Klebsiella pneumoniae bacteria in ankylosing spondylitis patients with/without extra-articular features. 861 22

We measured IgA1 and IgA2 subclass antibody levels against human type I, II, III and IV collagens in patients with ankylosing spondylitis (AS) by enzyme linked immunosorbent assay (ELISA). Significant elevations of IgA1 antibodies against type II collagen (p < 0.01) and IgA2 antibodies against type I (p < 0.001), III (p < 0.001), and IV (p < 0.01) collagens were observed in AS patients compared with those of healthy controls. These findings suggest that serum IgA antibodies against type I, III and IV collagens were mainly produced in secretory lesions in AS patients.
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PMID:Serum IgA1 and IgA2 subclass antibodies against collagens in patients with ankylosing spondylitis. 938 51