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)

So as to distinguish the separate influences of ankylosing spondylitis (AS) and possible HLA B27 associated immune response genes on immune response patterns, a battery of immunological tests were performed on fourteen patients with AS and their first-degree relatives. Previously unrecognized AS was detected by clinical and radiological means. Individuals with ankylosing spondylitis had significantly higher serum IgG and IgA concentrations than both their B27 positive and B27 negative relatives. B27 positive relatives had significantly lower phytohaemagglutinin (PHA) lymphocyte transformations than B27 negative relatives (P less than 0.01), while there was no difference between the ankylosing spondylitic and B27 positive groups. Antibody titres to Streptokinase/Streptodornase were significantly higher in the B27 positive individuals, with or without AS, than their B27 negative relatives (P less than 0.005 and P less than 0.02 respectively). These results show that serum immunoglobulin differences were associated with disease, while differences in PHA stimulation and varidase antibody titres were associated with the B27 antigen. These findings may indicate the presence of HLA associated immune response genes including those involved with reactions to a particular antigenic component of Streptokinase/Streptodornase.
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PMID:Immune function in ankylosing spondylitics and their relatives: influence of disease and HLA B27. 10 77

Presence of anti-lipoprotein activity, a new serological finding in inflammatory rheumatoid disease, has been established in sera and synovial fluids of 20 patients, among which were 6 cases of ankylosing spondylitis. In 18 of the patients, sera were negative for rheumatoid factor. Anti-lipoprotein activity can best be demonstrated by the hemagglutination technique. The binding activity is directed against autologous as well as homologous, however not against heterologous HDL and LDL. It has no specificity for Ag factors. Anti-LDL activity can also be demonstrated by means of double-diffusion tests, whereas no agar-precipitation has been noticeable using HDL as the antigen. Lipoprotein binding-activities were shown to be localized in the Fab fragments of IgG and, in 2 of the cases, also in IgA. We therefore assume that the underlying mechanism of the antilipoprotein activity is auto-immunization, despite of the fact that neither activation of complement nor a stoichiometric character of the binding reaction could be ascertained. Because hemagglutination and immunoprecipitation tests, respectively, were postive with apo-HDL und apo-LDL too, we consider the apo-protein to carry the antigenic site of the reaction. Sera with anti-lipoprotein autoantibodies from patients with chronic rheumatoid disease also presented another pecularity, i.e., a significant decrease of total lipids, cholesterol, and other components of the lipid spectrum. In patients with paraproteinemia, a similar combination of lipoprotein-binding activity and hypolipidemia or hypocholesterolemia was discussed in a previous paper. Regarding the pathogenesis of hypolipidemia or hypocholesterolemia in our patients with rheumatoid disorders, results of LDL turnover studies were indicative for an increase of the lipoprotein catabolism in the presence of anti-lipoprotein autoantibodies, together with a shift of the intra-extravascular distribution toward the intravascular pool. We assume the increased lipoprotein catabolism in these cases to be due to a trapping of lipoproteins by autoantibodies, and to accelerated degradation of these immune complexes. From a practical point of view, it may be of clinical importance that this new serological finding has been observed mainly in patients with chronic rheumatoid disease lacking a rheumatoid serum factor, and was frequently found in patients with ankylosing spondylitis (6 out of the 20 cases). As a screening method, we recommend systematic determinations of the total lipids and of serum cholesterol in all patients with inflammatory rheumatoid disease. In cases with low levels of total lipids and cholesterol, respectively, it may be useful to search for anti-lipoprotein autoantibodies using the hemagglutination method. Results are reported from some preliminary experiments on animals elicitation of an arthritis by means of intra-articular injections of autologous apo-HDL and apo-LDL, and demonstration of autoantibodies against HDL and LDL).
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PMID:[Anti-lipoprotein autoantibodies with hypolipidemia in infectious rheumatism]. 16 37

A patient with ankylosing spondylitis was found to have selective IgA deficiency and a non-heparin, immediate-acting antithrombin (antithrombin V). T cells were decreased, and serum IgG was increased. In vitro synthesis of IgG by peripheral blood lymphocytes was very high. This association of ankylosing spondylitis with the T cell and protein abnormalities is probably fortuitous but does demonstrate that severe spondylitis may evolve in the absence of IgA.
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PMID:Ankylosing spondylitis with selective IgA deficiency and a circulating anticoagulant. 92 6

Serum levels of C4, C3, IgG, IgM and IgA were measured by immunodiffusion in age matched groups of 48 sporadically encountered patients with ankylosing spondylitis, 56 with rheumatoid arthritis and 52 normal controls. Mean levels of C4 and IgA were significantly elevated in the sera of patients with sporadic ankylosing spondylitis, in comparison to normal controls. Mean IgA levels were also significantly elevated in 11 HL-A 27 positive patients with familial spondylitis but no such elevation was found in the sera of their healthy first-degree relatives with and without HL-A 27. The results of these studies suggest that humoral immune mechanisms may be involved in the pathophysiology of ankylosing spondylitis.
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PMID:Serum complement and immunoglobulin levels in sporadic and familial ankylosing spondylitis. 118 43

Antibodies to the collagen-like region of C1q have been described in patients with SLE and rheumatoid vasculitis. In this study the prevalence of both IgG and IgA C1qAb was assessed in serum samples of 385 patients with different systemic and renal diseases. The results demonstrate that the prevalence of IgG and IgA C1qAb is not restricted to the diseases in which they were originally described. C1qAb can also be demonstrated in patients with MCTD, Felty's syndrome, ankylosing spondylitis, polyarteritis nodosa, mixed cryoglobulinaemia, membranoproliferative glomerulonephritis, glomerulosclerosis, and patients with anti-glomerular basement membrane nephritis. The widespread occurrence of C1qAb of both immunoglobulin classes in systemic and renal diseases may provide insight into the mechanisms that lead to C1qAb formation.
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PMID:IgG and IgA autoantibodies to C1q in systemic and renal diseases. 134 21

Whole gut lavage fluid is a useful source of material for the study of intestinal immunity and inflammation in humans. Systemic and mucosal antibodies to Klebsiella pneumoniae were measured by enzyme linked immunosorbent assay (ELISA) in serum samples and whole gut lavage fluid from 14 patients with ankylosing spondylitis, 14 with Crohn's disease, and 16 immunologically normal controls. As the concentration of IgG in whole gut lavage fluid reflects disease activity in Crohn's disease, this approach was used to detect intestinal inflammation in patients with ankylosing spondylitis who also had disease activity and use of non-steroidal anti-inflammatory drugs (NSAIDs) recorded. Small intestinal permeability to cellobiose and mannitol was also studied. In serum samples, levels of IgA antibody to klebsiella were high in patients with Crohn's disease and in patients with active ankylosing spondylitis, and were significantly correlated with the erythrocyte sedimentation rate in patients with ankylosing spondylitis. Levels of IgG antibody to klebsiella were also high in patients with Crohn's disease. Studies of whole gut lavage fluid showed similar levels of IgA antibody to klebsiella in the three study groups, but levels of whole gut lavage fluid IgM and IgG antibodies to klebsiella were high in patients with Crohn's disease. Levels of IgG in whole gut lavage fluid were high in patients with Crohn's disease but in only one patient with ankylosing spondylitis, though the cellobiose/mannitol permeability ratio was abnormal in eight of 13 patients with ankylosing spondylitis. It is concluded that high levels of serum IgA antibody to klebsiella are not specific to ankylosing spondylitis, and that there is no evidence of an abnormal intestinal IgA antibody response to klebsiella in patients with ankylosing spondylitis.
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PMID:Systemic and mucosal antibodies to Klebsiella in patients with ankylosing spondylitis and Crohn's disease. 148 10

Three patients, all exhibiting symptoms before 15 years of age, were diagnosed as juvenile ankylosing spondylitis (JAS) by stigma of JAS. The families of these three patients--a total of fifteen first-degree relatives--had clinical, radiologic and laboratory examinations. All three patients and four family members (26%) had positive HLA-B27 and ankylosing spondylitis (AS). Five (33%) of these three family members had positive HLA-B27 but were asymptomatic; six members(40%) were HLA-B27 negative and symptom-free. A high positive rate of HLA-B27 was found among the patients (100%) and the family members (60%). The rheumatoid factor, antinuclear antibody, and anti-native DNA antibody were negative for all patients and family members. Significant elevation of IgG, IgA, and C3 were noted in the AS group. The CD3 cell was lower, and the ratio of CD4/CD8 was decreased in the AS group. Lympho-proliferative responses to phytomitogens (Con A, LPS and PHA) were also done in our study. There was no significant difference in Con A and LPS stimulation index among the AS group, symptom-free family members and normal controls.
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PMID:Immunological study in three families of juvenile ankylosing spondylitis. 151 12

Immune complexes have been reported in ankylosing spondylitis (AS) and may implicate infectious agents. Serum samples from 49 patients with AS were assayed for immune complexes by polyethylene glycol precipitation, followed by radial immunodiffusion and pepsinogen binding immunoassay. Both methods showed increases in IgA containing immune complexes, which correlated with serum IgA and with IgA rheumatoid factor concentrations, but did not show increases in other immune complex components. Increased immune complexes were associated with peripheral joint synovitis, but showed no correlation with other clinical or laboratory indices of disease activity. Immune complexes from nine AS serum samples and one AS synovial fluid were electrophoretically separated then probed with anti-Klebsiella pneumoniae, but AS specific antigens were not identified. This study did not suggest a major role for immune complexes in AS without peripheral disease, nor provide serological evidence for the involvement of klebsiella antigens.
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PMID:Immune complexes in ankylosing spondylitis. 154 45

IgA antibodies to Klebsiella pneumoniae var oxytoca and Proteus mirabilis were measured in 66 patients with ankylosing spondylitis (AS) and 31 with rheumatoid arthritis (RA) and in 51 healthy control subjects, using an immunoblotting technique. The number of antigenic bands to klebsiella on nitrocellulose membrane was higher in 28 patients with active AS than in 38 patients with inactive AS, 31 patients with RA, and 51 healthy control subjects; comparatively smaller increases were found against proteus. In two patients with AS the synovial fluid and the corresponding serum sample showed an identical antibody pattern. Increases in IgA antibodies to klebsiella in patients with AS confirm previous studies using other techniques.
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PMID:IgA antibody response to klebsiella in ankylosing spondylitis measured by immunoblotting. 155 Apr 9

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


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