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)

The importance of HLA-B27 in the pathogenesis of ankylosing spondylitis is uncertain: current evidence favours a role for the B27 molecule itself. The possibility that quantitative differences in HLA-B27 expression may exist between patients with ankylosing spondylitis, family members, and control subjects positive for B27 was examined using appropriate monoclonal antibodies, flow cytometry, and a 'model lymphocyte' coated with a known number of mouse immunoglobulin binding sites. No differences were found between the groups. HLA-A2, examined for comparison, was expressed in greater amounts than HLA-B27, but each contributed only 10-20% of the total class I antigens. Homozygotes expressed twice the amount of antigen expressed by heterozygotes. Synovial lymphocytes expressed more class I antigens than peripheral lymphocytes.
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PMID:Measurement of HLA class I expression in ankylosing spondylitis. 144 27

The association of HLA-B27 with ankylosing spondylitis and related spondyloarthropathies has been known for two decades and has provided a great impetus to the epidemiologic studies and also helped broaden the clinical spectrum of these diseases. The etiology of these diseases is likely to be multifactorial and include genetic, immunologic, and environmental mechanisms. The detailed three-dimensional x-ray crystallographic structure of B27 has now been reported. It has revealed electron density compatible with oligopeptides that are nine amino acid-long (nonamers) bound in the antigen-binding cleft of the molecule. Microsequence analysis of 11 peptides eluted from the antigen-binding cleft has confirmed that all are nonamers. The most restricted position in the bound peptide is the second position, where all the 11 peptides contain arginine. The side chain of arginine extends into the B pocket ("45 pocket"), which seems to act as a specificity side pocket in the antigen-binding cleft of the B27 molecule. It is very likely that an understanding of the detailed structure of B27, including the peptide-binding motif and the structural domains recognized by cytotoxic T cells, along with the recent development of the B27 transgenic rat model for spondyloarthropathies, will further enhance our understanding of the immunogenetics of these diseases. It is hoped that this will lead to the source of the arthritogenic triggers and possibly disease prevention by antigen-specific immunomodulation. Because T-cell activation is initiated by the formation of antigen-MHC complexes that are the ligands that are recognized by the antigen-specific T-cell receptor (TCR), it might be possible to inhibit this activation by blocking the antigen-binding cleft of MHC molecules by using high-affinity MHC-binding peptides (MHC blockade) or by a novel, new, and more efficient method of TCR antagonism.
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PMID:Immunogenetics of spondyloarthropathies. 145 47

A population survey of the Sami (Lapp) population of the municipalities Karasjok and Kautokeino in north Norway revealed a prevalence of ankylosing spondylitis (AS) according to the New York criteria of 1.8%. Eleven cases of AS were found, 7 men and 4 women. Only 4 of the 11 observed cases of AS were aware of the diagnosis of AS prior to the survey. Ten of 11 patients with AS possessed HLA-B27 (91%) which is found in 24% of the general Sami population in this area. It was calculated that 6.8% of B27 positive persons had AS.
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PMID:The prevalence of ankylosing spondylitis among Norwegian Samis (Lapps). 146 73

The association between three major spondyloarthritic diseases, ankylosing spondylitis, Reiter's syndrome, and reactive arthritis, and the major histocompatibility complex (MHC) class 1 antigen HLA-B27 is well documented. The hypothesis of cross-reactivity between HLA-B27 and the antecedent infection-causing Gram-negative pathogens such as Salmonella, Shigella and Yersinia has been suggested by in vitro studies employing monoclonal antibodies. We have examined the possibility of such cross-reactivity in vivo using various rabbit immune sera and patient sera as the source of cross-reacting antibody. Mouse L cells were transfected with HLA-A3 or HLA-B27 and used as a source of antigen. Western blot analysis employing denatured antigen, FACS analysis employing native antigen and immunoprecipitation studies were undertaken to detect cross-reacting antibodies generated in vivo to HLA-B27 antigen. Antibodies generated in vivo by infection in patients or immunization in animals against arthritogenic bacteria did not demonstrate any cross-reactivity with HLA-B27 by any of the methods used. As defined by the humoral immune response, molecular mimicry appears unlikely to explain the role of B27 in the pathogenesis of reactive arthritis.
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PMID:HLA-B27/microbial mimicry: an in vivo analysis. 147 90

Several authors have suggested that immunoglobulin A plays a pathogenic role in ankylosing spondylitis. We have determined the levels of immunoglobulins in 30 patients, observing higher levels than in control patients (248 vs 176 mg/dl); p less than 0.01) and a relation between the increase of immunoglobulin A and the presence of clinical activity in the subgroup of patients B27-negative (163 vs 398 mg/dl, p less than 0.005), but not in B27-positive patients. We think that these e results support the hypothesis that ankylosing spondylitis is an heterogeneous disease, with different pathogenic mechanisms depending on the presence or absence of the serological marker HLA-B27.
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PMID:[Clinical activity and serum immunoglobulin concentrations in patients with ankylosing spondylitis]. 150 1

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

The author experienced a 34-year-old male case of acute iridocyclitis with fibrinous exudates accompanied by ankylosing spondylitis with negative HLA-B27. Who was diagnosed definite ankylosing spondylitis by the New York criteria. The cause of ankylosing spondylitis was postulated to be a cross reaction between HLA-B27 and a certain Gram-negative bacillus. However, our case with negative HLA-B27 suggested the causes could comprise multiple factors in addition to HLA-B27. Since the clinical picture of iridocyclitis observed in our case showed no difference with those of HLA-B27 positive cases, iridocyclitis associated with ankylosing spondylitis is considered to be the same entity regardless of HLA-B27 being present or not.
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PMID:[An HLA-B27 negative case of ankylosing spondylitis with acute iridocyclitis]. 155 26

Ankylosing spondylitis is a form of reactive arthritis following Klebsiella infection, usually occurring in an HLA-B27-positive individual. This conclusion is based on evidence obtained from several disciplines: immunogenetic studies show that there is molecular mimicry between HLA-B27 and Klebsiella; increased isolation of fecal Klebsiella has been reported in both Europe and North America; and finally, antibodies to Klebsiella have been demonstrated in ankylosing spondylitis patients in England and Finland. It is suggested that therapeutic trials should be set up with the aim of eliminating Klebsiella microbes, in an endeavor to test the validity of this theory.
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PMID:Ankylosing spondylitis is caused by Klebsiella. Evidence from immunogenetic, microbiologic, and serologic studies. 156 97

An acute onset, unilateral anterior uveitis occurs during the course of either Reiter's syndrome or ankylosing spondylitis. Conversely, many patients who suffer from an acute anterior uveitis are HLA-B27-positive and have associated joint disease. The consistent presentation of the uveitis can aid in the process of differential diagnosis. This article includes a discussion of the recognition of the characteristic presentation, the complications, the role of B27 testing, the relevance of animal models, the pathogenesis, and treatment.
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PMID:Acute anterior uveitis and spondyloarthropathies. 156

Seventy-nine consecutive patients with active ulcerative colitis were studied to establish the prevalence and clinical features of articular involvement. HLA typing for A and B loci was performed. Forty-nine patients showed an articular involvement (62%). Three different clinical patterns were identified: ankylosing spondylitis occurring in 20 subjects; peripheral arthritis in 15; unclassifiable spondylitis in 14. When compared to the general population in our area, patients with colitis showed a significantly higher prevalence of the HLA-A1 (p less than 0.005), B21 (p less than 0.001) and B27 (p less than 0.05); among patients with colitis, those with arthritis revealed higher frequency of HLA-B27 (p less than 0.05). Our study reveals a high prevalence of unclassifiable spondylitis during ulcerative colitis, and suggests a new approach to the classification of seronegative spondarthritis.
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PMID:The arthritis of ulcerative colitis: clinical and genetic aspects. 157 50


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