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)

Sera from 50 patients with various stages of ankylosing spondylitis were tested for the presence of antinuclear antibodies (ANA), anti-DNA antibodies, rheumatoid factor and antistreptolysin. Antinuclear antibodies (immunofluorescent technique) were detected in the sera of 10 patients (20%), associated in one case with anti-DNA antibodies (immunofluorescent technique). The disease activity in ANA-positive cases was low to moderate.
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PMID:[Immunological features in ankylosing spondylitis (author's transl)]. 30 86

Elevated natural radioactivity during a treatment at Badgastein (Austria) caused an increase in DNA-repair of lymphocytes of patients with ankylosing spondylitis and osteoarthritis. Semiconservative DNA-synthesis was remarkably lower after the treatment in patients with ankylosing spondylitis and a small decrease was obtained also in lymphocytes of osteoarthritis patients. These effects are discussed in relation to late effects.
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PMID:[DNA-synthesis and DNA-repair in chronic rheumatism influenced by small doses of natural radioactivity (radon)]. 62 91

The somatomedin activity in synovial fluids from 50 patients with a variety of joint diseases has been studied and compared with the activity in each of the patient's own serum and a standard reference serum (SRS). The porcine costal cartilage bioassay of Van den Brande and Du Caju (1974a) has been used with the isotopes 3H-thymidine and 35S-sulphate. Synovial fluids from most patients with post-traumatic and post-operative effusions, osteoarthritis and arthritis associated with psoriasis, Reiter's disease, and ankylosing spondylitis stimulated the synthesis of DNA and proteoglycans in cartilage. Synovial fluids from patients with rheumatoid arthritis either had impaired capacity to stimulate DNA synthesis, or they inhibited it; a similar, but less evident pattern was observed for proteoglycan synthesis. Some synovial fluids from patients with miscellaneous synovitides stimulated, while others inhibited cartilage metabolism. It is concluded that the synovial fluid from patients with rheumatoid arthritis and from some patients with miscellaneous synovitides contained an inhibitor(s) to DNA and possibly proteoglycan synthesis. The sera from nearly all the patients stimulated both DNA and proteoglycan synthesis, but the somatomedin potency ratios for serum in terms of SRS were generally less than 1.0. There was a significant inverse correlation between the serum somatomedin potency ratio and the age of the patient.
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PMID:Somatomedin activity in synovial fluid from patients with joint diseases. 68 63

Sera of children with juvenile rheumatoid arthritis and other connective tissue diseases were tested for antibodies to native DNA by a radiolabeled-binding assay. Normal values were obtained in 130 children with JRA, including 28 with uveitis and 14 with selective IgA deficiency. Normal values were also found in sera from children with dermatomyositis, scleroderma, polyarteritis, ankylosing spondylitis, and a variety of other nonconnective tissue diseases. The only sera with elevated DNA-binding assays were from children with systemic lupus erythematosus. On the basis of these data, increased levels of antibodies to native DNA distinguished patients with active SLE from children with JRA.
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PMID:Diagnostic significance of antibody to native deoxyribonucleic acid in children with juvenile rheumatoid arthritis and other connective tissue diseases. 69 Jul 54

Human lysosomes were isolated from normal peripheral blood leukoyctes and characterized by electron microscopy, enzyme analysis, and assays for DNA and RNA. Stored sera from 37 unselected patients with systemic lupus erythematosus (SLE), including active and inactive, treated and untreated cases, were tested in complement fixation (CF) reactions with these lysosome preparations. 23 SLE sera exhibited positive CR reactions, as did sera from two patients with "lupoid" hepatitis. The seven SLE sera with strongest CF reactivity also demonstrated gel precipitin reactions with lysosomes. Neither CF nor precipitin reactions with lysosomes were observed with normal sera or with sera of patients with drug-induced lupus syndrome, rheumatoid arthritis (RA), polymyositis, or autoimmune hemolytic anemia. By several criteria the antilysosome CF and precipitin reactions of SLE sera cound not be attributed to antibody to DNA, RNA, or other intracellular organelles. The lysosomal component reactive with SLE sera in CF assays was sedimentable at high speed and is presumably membrane associated. The CF activity of two representative SLE sera was associated with IgG globulins by Sephadex filtration. A search for lysosomal antigen in SLE and related disorders was also made. By employing rabbit antiserum to human lysosomes in immunodiffusion, a soluble lysosomal component, apparently distinct from the sedimentable (membrane-associated) antigen described above, was identified in serum, synovial fluid, or pleural fluid from patients with SLE, RA, ankylosing spondylitis, and leukemoid reaction. An antigenically identical soluble component reactive with the rabbit antiserum could be released in vitro from intact lysosomes by repeated freeze-thaw cycles..
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PMID:Studies with human leukocyte lysosomes. Evidence for antilysosome antibodies in lupus erythematosus and for the presence of lysosomal antigen in inflammatory diseases. 109 14

Several studies of DNA restriction fragment length polymorphism (RFLP) in ankylosing spondylitis (AS) have been carried out. The association between a recently identified class I HLA 9.2 kb PvuII RFLP and AS remain controversial. In order to evaluate this possible association in an Euro-Caucasian population, the genomic DNA of 42 AS patients and 18 patients with Reiter's syndrome (RS) and 42 healthy controls was analysed. Non-association between 9.2 kb PvuII RFLP and AS or RS was observed. As described previously, a strong association between this fragment and HLA-A3 and/or HLA-A9 antigens was demonstrated. A study of two families showed that this RFLP segregates with HLA-A3 and/or HLA-A9 and independently of the HLA-B27. Our findings support the view that the 9.2 kb PvuII fragment is not universally associated with AS.
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PMID:Non-association between 9.2 KB PvuII RFLP and seronegative spondyloarthropathies in Spain. 136 Mar 7

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

Antigen processing for presentation of peptide epitopes by major histocompatibility complex (MHC) class I molecules involves genes in the MHC class II region. Among these, PSF1 and PSF2 encode subunits of a transporter, which presumably delivers cytosolic peptides across the endoplasmic reticulum membrane to class I molecules. This close functional relationship of the transporter and class I heavy chain genes and their linkage within the MHC raise the question of whether PSF1 and PSF2, like most class I genes, are polymorphic. By single-strand conformation polymorphism analysis and DNA sequencing, a small number of amino acid sequence variants of both PSF1 and PSF2 was identified in a panel of cell lines. This limited polymorphism may contribute to a higher degree of variability at the level of the functional transporter, in which different alleles of the PSF1 and PSF2 subunits may be combined. A possible involvement of the PSF1 and PSF2 genes in susceptibility to MHC-associated diseases was examined in a preliminary assessment in patients with ankylosing spondylitis, insulin-dependent diabetes mellitus, or celiac disease.
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PMID:Allelic variants of the human putative peptide transporter involved in antigen processing. 157 Mar 16

HLA-B27 is strongly associated with susceptibility to ankylosing spondylitis and other spondyloarthropathies. Structural analysis of this antigen has revealed the existence of multiple variants, or subtypes, in human populations. The structural microheterogeneity of these subtypes deeply affects allospecific T cell recognition and most of it occurs at an spatial cluster within the peptide binding groove of the molecule. Many polymorphic residues whose combination is unique to HLA-B27 but is conserved among subtypes are clustered in a spatially separated site of the groove from that where most subtype polymorphism occurs. Site-directed mutagenesis and DNA-mediated gene transfer has been used to show that the positions that are polymorphic among subtypes are highly relevant for modulating T cell recognition, so that immunologically silent changes do not occur. These studies have also revealed an extremely high clonotypic diversity in the alloreactive response against HLA-B27. The structural basis for this diversity has been examined by sequencing the clonotypic T cell receptors. The analysis shows a certain bias in V beta gene segment usage, as well as other recurrent structural motives, among T cell receptor beta chains from HLA-B27-specific cytotoxic T cell clones.
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PMID:Structure and immune recognition of HLA-B27 antigens: implications for disease association. 170 18

The authors have used the modified method of the direct gene cloning suggested by Nichols et al to isolate HLA-B27 gene from a patient suffering from ankylosing spondylitis. Five restriction enzymes (ClaI, HindIII, SnaBI, PvuI, SalGI) which had no recognition sites within the 6.0 kb EcoRI-BamHI-DNA fragment supposedly containing the HLA-B27 gene have been chosen by blotting-hybridization of the restriction fragments of the patients DNA with HLA-B27-specific probe. The 6.0 +/- 0.5 kb DNA fragments were isolated and cloned after the DNA treatment by 300 micrograms of all of these restriction enzymes. The obtained mini-library containing 280 recombinants has been screened with the use of HLA-B27 specific oligonucleotide probe. The clone PB27-2 has been isolated the restriction map of which is identical to HLA-B27k. The authors are planning to determine the sequence of the isolated gene in order to find a possible structural defect in it.
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PMID:[Directed cloning of the HLA-B27 gene isolated from a patient with ankylosing spondylitis (Bechterew's disease)]. 223 90


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