Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0003864 (arthritis)
 69,039 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Synovial fluid mononuclear cells (SFMC) from patients with reactive arthritis (ReA) show marked proliferative responses to preparations of the organism triggering the arthritis. Initial studies with MHC-specific MoAbs have indicated that a significant element of these proliferative responses is mediated by class II MHC-restricted CD4+ T cells. It is imperative to establish the presence or absence of a class I-restricted response, for two reasons. Firstly, the association of ReA with the MHC class I molecule, HLA B27, raises the possibility of there being a B27-restricted response to the triggering organism. Secondly, a number of the organisms associated with ReA are intracellular pathogens, whose antigens might be expected to be presented by class I MHC molecules. In an effort to identify a class I MHC-restricted pathogen-specific response in the SFMC of ReA patients, we have assessed the proliferative responses of SFMC depleted of CD4+ T cells. Responses were grossly diminished by CD4+ T cell depletion. We also investigated Chlamydia-specific cytotoxicity in the SFMC of patients with sexually acquired ReA in a system using productive chlamydial infection to produce both targets and effectors. Significant antigen specific cytotoxicity was not seen. These experiments do not provide evidence to support the existence of pathogen-specific responses by CD8+, class I-restricted synovial fluid T cells in ReA.
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PMID:MHC restriction of synovial fluid lymphocyte responses to the triggering organism in reactive arthritis. Absence of a class I-restricted response. 160 28

HLA B27 and other clinical findings were investigated in 18 Turkish patients with Reiter's syndrome (mean age 35.8 +/- 8.09). Male/female ratio was 2/1. All 18 patients were seronegative, 12 (66.6%) presenting with an asymmetrical oligoarticular arthritis. Radiological sacroiliitis and enthesopathy was found in 9 (50%) and 7 (45.6%) patients respectively. HLA B27 was present in 11 (61.1%) patients.
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PMID:HLA B27 and clinical features in Reiter's syndrome. 161

Following a foodborne outbreak of Salmonella dysentery in a group of 79 women and 4 men, 6 individuals were found to have reactive arthritis (ReA). None of the affected individuals had the classical genetic marker HLA B27 although 2 of the 6 had CREG antigens. IgA antibodies to the lipopolysaccharide of the causative organism, Salmonella heidelberg, were found to be elevated in those patients with active ReA compared to those with inactive ReA or those who had dysentery but did not develop ReA. The lymphocyte proliferative response to both PHA and the whole S. heidelberg organism was impaired in the patients with ReA (active or inactive) compared with the non-ReA patient controls. In this predominantly female outbreak of Salmonellosis, the development of ReA lacked an association with HLA class I antigens commonly recognized.
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PMID:Immunoepidemiology of post-Salmonella reactive arthritis in a cohort of women. 164 56

Although ankylosing spondylitis (AS) is known to be strongly associated with the class I major histocompatibility complex antigen HLA-B27, B27 is probably not the only genetic factor involved in the pathogenesis of AS. Because of the involvement of tumor necrosis factor (TNF) in cartilage damage and the localization of the TNF genes in the proximity of the HLA-B locus, we investigated the association between AS and TNF alleles. The frequencies of the restriction fragment length polymorphisms linked to the TNF genes were determined in 73 AS patients and 81 controls. No differences were observed between AS patients and controls with respect to the frequencies of the TNF restriction fragment length polymorphisms.
Arthritis Rheum 1991 Apr
PMID:Restriction fragment length polymorphism of the tumor necrosis factor region in patients with ankylosing spondylitis. 167 16

In this multicentre pilot study of sulphasalazine in juvenile chronic arthritis, the mode of onset and course of the disease, and when available, the HLA status, was recorded on the entry form. After appropriate clinical and laboratory appraisal, sulphasalazine up to 40 mg/kg/day was given for one year with assessments at 0, 1, 3, 6, 9 and 12 months. Fifty-one patients enrolled, 8 of whom were withdrawn because of side effects. In the remainder by 12 months a good effect was noted in 12, 8 having pauci-articular onset disease commencing after the age of 9 years, of whom 6 carried HLA B27. It was relatively ineffective in the other subgroups. The frequency and severity of side effects was similar to that seen in adults. Further evaluation in controlled trials is required in older onset pauci-articular arthritis, taking due note of the patient's HLA status, and also in juvenile psoriatic arthritis and seropositive juvenile rheumatoid arthritis.
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PMID:A multicentre pilot study of sulphasalazine in juvenile chronic arthritis. 167 52

The phenotype HLA-B27 is common in patients who develop reactive arthritis after having an infection. One hypothesis concerning the pathogenesis of reactive arthritis is that molecular mimicry between HLA-B27 and certain bacterial components might be involved. It is known that an infection with Yersinia is commonly associated with reactive arthritis in B27 positive patients. Therefore, we were interested to investigate whether cross-reactivity between Yersinia and HLA-B27 exists. A gene library of Yersinia pseudotuberculosis was created in the plasmid vector pUC13. One of the resulting clones contained a gene encoding an intracytoplasmic protein that seems to have partial epitope identity with HLA-B27. It reacted in western blot. ELISA and immunoprecipitation with three different HLA-B27 specific monoclonal and polyclonal antibodies of the IgG and IgM class. However DNA-sequencing of the cloned Yersinia gene and the predicted amino acid sequence revealed only a very remote similarity with HLA-B27 in the primary structure. Instead, an extremely high degree of similarity with the ribosomal protein L4 of the S10 operon of Escherichia coli was identified indicating that the protein encoded by the cloned Y. pseudotuberculosis gene is a corresponding ribosomal protein.
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PMID:A ribosomal protein of Yersinia pseudotuberculosis having partial epitope identity with HLA-B27. 171 96

Two new examples of amino acid homology between HLA B27 and microbes triggering HLA B27-associated diseases are described. An outer membrane protein YadA (Yersinia adhesin, previously called Yop1) of Yersinia enterocolitica and Y. pseudotuberculosis shares a linear tetrapeptide with HLA B27. A cationic outer membrane protein OmpH of Salmonella typhimurium shares homology with five amino acids of HLA B27 in a non-linear fashion. The four amino acids of YadA are also notably included in the hexapeptide identical between Klebsiella pneumoniae nitrogenase and HLA B27, and three of them occur in the pentapeptide shared by a Shigella flexneri protein and HLA B27. Antibodies against synthetic peptides including HLA B27 homologues sequences of YadA and OmpH were observed in one-third of the patients with HLA B27 associated diseases. Antibodies were directed against a flanking sequence next to the amino acid sequences shared by arthritis-triggering microbes and HLA B27. The area of identity in each example of this molecular mimicry (Yersinia, Salmonella, Shigella and Klebsiella) is located in the same place on the HLA B27 molecule: between amino acids 70 to 78 in the variable region of alpha 1-helix. This area of HLA B27 molecule includes sites predicted to be important for binding processed antigens.
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PMID:Molecular mimickry between HLA B27 and Yersinia, Salmonella, Shigella and Klebsiella within the same region of HLA alpha 1-helix. 174 48

Interleukin-6 (IL-6) concentrations in knee joint synovial fluids and paired plasma samples of arthritis patients were examined with respect to each other and parameters of the inflammatory response. Synovial fluid and plasma IL-6 concentrations were significantly higher in patients with inflammatory arthritis than those detected in patients with osteoarthritis (P less than 0.001). The IL-6 concentrations in synovial fluids were considerably higher than, but significantly correlated with (r = 0.65; P less than 0.001), those of plasma. Furthermore, synovial fluid IL-6 concentrations in bilaterally inflamed knees were significantly correlated (r = 0.79; P less than 0.001) and there was a significant correlation with the extent of inflammatory cell infiltrate (r = 0.75; P less than 0.001). In unselected rheumatoid arthritis patients there was only a weak correlation between IL-6 and plasma C-reactive protein (CRP) concentration, and no correlation between IL-6 and erythrocyte sedimentation rate (ESR). However, both ESR and CRP concentration were highly correlated with plasma IL-6 concentration in patients with other inflammatory arthritides, particularly psoriatic and HLA B27 positive spondyloarthritis (r = 0.72-0.94; P less than 0.005). These relationships suggest that IL-6 production in inflammed knee joints can be a significant determinant of acute phase protein responses in arthritis patients, although the situation in patients with rheumatoid arthritis is more complex and may be influenced by other disease-related factors.
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PMID:Relationships between local inflammation, interleukin-6 concentration and the acute phase protein response in arthritis patients. 175 86

Juvenile rheumatoid arthritis (JRA) is a chronic, relapsing, inflammatory childhood disease characterized by arthritis and systemic inflammation. At present there is no rapid, efficient laboratory method of assessing disease activity and degree of immune activation. We measured serum soluble interleukin 2 receptor (sIL-2R) levels in 85 samples from 72 patients (22 samples from patients with systemic JRA, 34 from polyarticular patients, 29 from pauciarticular patients, of which 10 were HLA-B27 positive). The mean sIL-2R level from patients was 1565 U/ml, which is significantly elevated compared to control values of 594 U/ml (p less than or equal to 0.005). The highest levels were seen in patients with systemic JRA (mean value 2121 U/ml) while the lowest values were seen in HLA-B27 positive (+) patients (mean value 899 U/ml). Patients with clinically active disease had significantly elevated levels (mean value 1745 U/ml) compared to patients with inactive disease (mean value 846 U/ml, p less than or equal to 0.01). Highest levels were seen in patients with active systemic JRA (mean value 2419 U/ml) while patients with pauciarticular JRA and B27 + JRA had the lowest sIL-2R levels (1167 and 1045 U/ml, respectively). sIL-2R levels were elevated in all subgroups of clinically active patients compared to controls (p less than or equal to 0.0005). Three of the 4 patients with serial sIL-2R measurements showed falling values during the period of clinical remission. Using regression analysis and likelihood ratio tests, we found a significant correlation between sIL-2R levels and both disease activity and joint count (p less than or equal to 0.005).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Soluble interleukin-2 receptor in juvenile rheumatoid arthritis. 175 44

HLA B27 antigen was found in 10/25 patients with arthritis after acute respiratory disease (ARD) and in 21/75 direct relatives of 23 of these probands, where a genealogical investigation could be made. With regard to the 9.5% incidence of HLA B27 in the Czech population this implies a positive association in patients (RR = 6.35) and direct relatives (R = 3.70). In the sub-group of HLA B27 positive probands HLA B27 positivity was found in 19/27 (70.4%) of direct relatives (RR = 22.6). In one female relative a recurrent monoarthritis of the talo-crural joint was found, the remainder did not suffer from inflammatory changes of the joints. The revealed positive associations indicate the probability of arthritis after ARD in HLA B27 positive subjects and their families. They indicate also that in arthritis after ARD reactive arthritis is involved with a less common organ manifestation of the initial infection.
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PMID:[HLA-B27 in the families of probands with arthritis after acute respiratory tract disease]. 177 11


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