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)

By serum typing, it is indicated that HLA B27 may be associated with the susceptibility to ankylosing spondylitis (AS). We analyzed DNA restriction fragment length polymorphism (RFLP) in 28 Chinese AS patients and 99 healthy controls, using a 1.4 Kb HLA class I cDNA probe. The results showed that the frequencies of the 8.1 Kb EcoRI, 5.2 Kb EcoRI and 21.9 Kb XbaI fragments were found to be significantly increased in affected patients (P less than 0.0001, P = 0.0015, respectively), but that of 19.2 Kb XbaI fragment was decreased (P = 0.0021). The data suggest that AS may be a polygenic disease; furthermore, B27 and 8.1 Kb EcoRI band may be two different factors responsible for the susceptibility or just in linkage disequilibrium with the susceptible gene(s).
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PMID:Association of RFLP of HLA class I genes with Chinese ankylosing spondylitis patients. 257 76

Genomic DNA from 46 B27+ ankylosing spondylitis, Reiter's syndrome, or normal individuals was digested with Taq I and probed, in Southern blots, with the HLA-B locus specific probe, EI7. Four restriction fragment length polymorphisms (RFLP), 2.5, 3.4, 3.8 and 4.0 or 8.0 kb, were observed for the B27 gene. In Caucasians, one of the B27 variants (2.5 kb) was more frequent in normals and almost never appeared in patients, suggesting a trend that is not yet statistically significant. In the course of defining the B27 polymorphisms, three and two RFLP, respectively, were also found for the B18 and B44 genes.
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PMID:New polymorphisms of HLA-B27 and other B locus antigens detected by RFLP using a locus-specific probe. 287 15

We analyzed DNA restriction fragment length polymorphism (RFLP) in 53 white ankylosing spondylitis (AS) patients and 92 healthy controls, utilizing a full-length HLA-B7 complementary DNA probe. A 9.2-kilobase (kb) Pvu II fragment was found to be significantly increased in frequency in B27 positive AS patients compared with the B27 positive control group (P = 0.00085, relative risk = 7.2). The presence of both B27 and the 9.2-kb RFLP in an individual conferred a relative risk for AS of 297, compared with a relative risk of 119 in those who had B27 alone. The 9.2-kb RFLP appears to be a marker for AS which, with HLA-B27, contributes further to susceptibility to the disease. Our findings indicate that this fragment and HLA-B27 segregate independently in familial studies of AS.
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PMID:Association of a 9.2-kilobase Pvu II class I major histocompatibility complex restriction fragment length polymorphism with ankylosing spondylitis. 288 67

Considerable evidence indicates that genes residing within the major histocompatibility complex (MHC) influence susceptibility to certain rheumatic diseases, such as ankylosing spondylitis (AS) and rheumatoid arthritis (RA). However, it has not yet been possible to precisely identify the gene(s) responsible for conferring enhanced susceptibility to these diseases. The availability of recombinant DNA technology should accelerate progress in obtaining this goal. A particularly promising method in this regard is restriction fragment length polymorphism (RFLP) analysis using appropriate class I and class II MHC gene probes. In preliminary studies, RFLPs have been identified for AS and RA which associate with susceptibility to the disease. Further studies using this approach should permit localization and precise identification of the disease susceptibility gene(s) for these diseases.
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PMID:Analysis of restriction fragment length polymorphisms in rheumatic diseases. 289 32

Twenty-nine patients with ankylosing spondylitis (AS) were studied in an attempt to evaluate the role of T lymphocytes in this disease and a possible influence of treatment. The proportions of various T cell subpopulations in blood were assessed with monoclonal antibodies. Before treatment the proportions of Leu-4+ cells and Leu 3a+ cells were decreased while Leu-2a+ lymphocytes appeared in normal proportions. Leu-7+ cells appeared in increased proportions. An increased proportion of Leu-M1 positive cells were identified in the lymphocyte preparation from the patients, possibly reflecting the presence of activated granulocytes. Activation of the different cell types was studied with double staining technique. No activated Leu-3a+ or Leu-2a+ lymphocytes were present in blood when the patients were analyzed as one group, but when divided into subgroups according to inflammatory activity, the highest levels of activated Leu-2a+ lymphocytes were found in the group with active disease. Functional assays measuring DNA synthesis of T and B cells were normal. After three months treatment with sulphasalazine the patients showed clinical and laboratory improvement. The proportion of activated Leu-2a+ cells decreased during treatment, but no other changes occurred in the lymphocyte markers or lymphocyte functional tests. A patient control group showed no clinical improvement nor any changes in T cell markers. Our results support the concept that AS is a disease which affects the lymphocyte system and that the improvement induced by sulphasalazine may involve actions on this system.
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PMID:T lymphocytes in ankylosing spondylitis and the influence of sulphasalazine treatment. 289 58

Recently, McDaniel, et al (Arthritis Rheum 1987;30:894) reported a statistically significant association between ankylosing spondylitis (AS) and the presence in Pvu II digested genomic DNA of a 9.2 kb restriction fragment hybridizing with an HLA-B7 cDNA probe. The fragment was found in 35 of 48 unrelated HLA-B27+ Caucasian patients with primary AS and in 25 of 107 controls. We report finding this restriction fragment in only 10 of 33 such patients and in 17 of 41 controls. We are thus unable to confirm an association between AS and the restriction fragment identified by McDaniel, et al.
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PMID:Association between ankylosing spondylitis and a 9.2 kb Pvu II class I HLA DNA restriction fragment: a reassessment. 256 78

A 435-kilobase (kb) DNA segment, which is centromeric to HLA-B in the human major histocompatibility complex, was isolated by chromosome walking with overlapping cosmids. Within the cloned region, the genes for the tumor necrosis factors (TNFs) alpha and beta and HLA-B were 210 kb apart. The human homolog of a mouse gene, B144, was located next to TNF alpha. Moreover, the presence of additional genes was suggested by a large cluster of CpG islands. With cosmid probes, several distinct transcripts were detected in RNA samples from a variety of cell lines. Altogether, five novel genes were identified by isolation of corresponding complementary DNA clones. These "HLA-B-associated transcripts" (BATs) were mapped to different locations within a 160-kb region that includes the genes for TNF alpha and TNF beta. The presence of the genes for BAT1 and BAT5 in the vicinity of HLA-B again raises the question of which gene in this region determines susceptibility to ankylosing spondylitis.
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PMID:A new cluster of genes within the human major histocompatibility complex. 291 34

The lymphocyte response of mononuclear cells (MNC) to Klebsiella (Klebs) was studied in ankylosing spondylitis (ASP) and, for comparison, in patients convalescing from Klebs infection and in HLA-B27+ and B27- healthy blood donors. When large doses of various Klebs cell envelope structures were used, MNC from all healthy blood donors were stimulated to produce LIF but not to synthesize significant amounts of DNA. In contrast, MNC from convalescent patients showed LIF synthesis (but no significant proliferation) even when small doses of the Klebs biostructures were used. This heightened LIF response to Klebs was long-standing and could be demonstrated even after serum antibodies had vanished. Very similarly, MNC from ASP patients did not proliferate significantly, but could be activated to produce LIF even with small doses of Klebs. The heightened LIF response to Klebs in ASP appeared to be correlated with the clinical activity and/or duration of the disease. In contrast, there was no correlation between the presence of HLA-B27 in ASP patients or healthy controls and the LIF or proliferative response to Klebs.
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PMID:Lymphocyte response to Klebsiella in ankylosing spondylitis. 310 Feb 99

Ninety percent of individuals with ankylosing spondylitis (AS) express HLA-B27. To determine if HLA-B27 coding sequences from normal vs AS individuals show differences that might relate to the etiology of the disease, the gene coding for this allele was cloned from three different partial genomic libraries. These libraries were made with DNA from three different cell lines expressing HLA-B27: MRWC (HLA-B27, 14), obtained from an AS patient; KCA (HLA-B27, w44), obtained from a known normal individual; and MVL (HLA-B27, 27), a homozygous consanguineous cell line of unknown origin. To increase the number of clones coding for the HLA-B locus, partial libraries were made using a complete Eco RI digestion of genomic DNA in the lambda vector 607. The libraries were screened with two probes; one probe hybridizes to all HLA-A, B, C class I genes, and the other to a small subpopulation of class I genes, including the B locus. DNA from clones hybridizing with both probes was transfected into murine L cells. Cell surface expression of HLA-B27 on murine L cells was detected with a polymorphic monoclonal antibody (ME1) specific for HLA-B27, 7, 22. DNA from those clones positive for HLA-B27 by transfection was subcloned into the Xba I site of M13mp18 and the DNA sequence for exons 2 through 4 (encoding domains alpha 1, alpha 2, and alpha 3) was determined by the dideoxy technique by using synthetic oligonucleotide primers or the M13 primer. The resulting sequences show no difference between HLA-B27 alpha 1, alpha 2, alpha 3 domains from a known AS patient and a known normal individual.
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PMID:Absence of polymorphism between HLA-B27 genomic exon sequences isolated from normal donors and ankylosing spondylitis patients. 348 55

Recent studies have indicated that both ankylosing spondylitis and the anti-DNA antibodies found in systemic lupus erythematosus may be related to Klebsiella surface antigens. In order to explore these possible relationships further, the sera of 24 patients with ankylosing spondylitis (AS), and 20 controls, have been examined for binding to a wide range of antipolynucleotide antibodies, antibodies binding to the Klebsiella pneumoniae polysaccharide K30 and two DNA antibody idiotypes designated 16/6 and 134. We report that although 21% of the AS patients had IgG ssDNA antibodies it is evident that the aetiopathogenesis of this disease is not through the mechanism of autoantibodies or the common DNA antibody idiotypes tested.
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PMID:A study of antipolynucleotide antibodies, anti-Klebsiella (K30) antibodies and anti-DNA antibody idiotypes in ankylosing spondylitis. 349 12


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