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)

26 HLA antigens of the loci A and B were studied in 50 patients with pseudo-polyarthritis and in 300 control subjects without any joint disease. The arthritis was isolated and not associated with temporal arteritis. An increase in frequency of both HLA antigens was noted in the patients studied: HLA-B5 = 24% as against 13% in controls (P = 0.05 and Pc NS). HLA-Bw38 = 18% as against 5.33% in controls (p = 0.002 - Pc = o.05). The rise in frequency of HLA-B5 and HLA-Bw38 was also found in 19 subjects with polyarthritis and temporal arteritis but not in 31 patients with temporal arteritis alone. In this disease, a link with the HLA-B14 antigen was noted in 50 cases (22.9% as against 8.6% in control). These results suggest that arthritis and temporal arteritis although sometimes associated are probably distinct diseases.
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PMID:[HLA system and rhizomelic pseudopolyarthritis]. 19 97

The frequencies of 21 HLA antigens in 33 patients who developed recurrent, episodic arthropathy after receiving the HPV-77 DK-12 rubella vaccine have been determined and compared with those of a control population. Trends toward increased frequencies of HLA antigens B12 (P = 0.02) and B14 (P = 0.04) and of the haplotype A2, B12 (P = 0.01) did not reach significance when corrections for the number of antigen determinations were included in the statistical analysis. These data show that the syndrome of recurrent arthropathy following rubella vaccination is genetically distinct from the connective tissue diseases associated with HLA-B27.
Arthritis Rheum
PMID:HLA and recurrent episodic arthropathy associated with rubella vaccination. 90 93

The authors report three cases of palmo-plantar pustulosis associated with articular signs: erosive arthritis of the right first sternocostal joint in 2 cases (without hypertrophy of the clavicle or the sternum) and atlanto-occipital arthropathy with marked neck stiffness in another case. The HLA phenotype of one case was: A2 - A9 - B14 - X - DR3 - DR4. A surgical sterno-costal biopsy revealed non-specific inflammatory lesions in 2 cases. In one of these cases, a Corynebacterium sp. was isolated. The clinical course was favourable in response to local antibiotic therapy in one case (follow-up of 8 years) and after treatment with non-steroidal anti-inflammatory agents in 2 cases (follow-up of one to two years). The skin biopsy revealed non-spongiform (and therefore non-psoriatic) unilocular pustulosis, distinguishing this non-bacterial pustulosis from pustular palmo-plantar psoriasis with which it is frequently confused. These cases are similar to the cases of "pustulotic arthro-osteitis" reported by Japanese authors (Sonozaki et al.), which appear to be rare in Europe. They seem to be an early form in a vast range of spondylo-arthropathies including rheumatism and acne conglobata. The aetio-pathogenesis of this syndrome is discussed; one of the cases is strongly suggestive of an infectious origin (Corynebacterium). These lesions do not appear to be a form of reactive arthritis, as the presence of HLA B27 is rare in both the European and the Japanese cases.
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PMID:[Anterior thoracic and intervertebral erosive joint diseases associated with palmoplantar pustulosis]. 404 9

We have previously demonstrated that the presence of the MHC class I molecule, HLA-B27, on the surface of transfected fibroblasts differentially alters Gram-negative bacterial invasion as compared with class I alleles that are not implicated in the seronegative spondyloarthropathies. We have now extended this analysis to show that fibroblasts transfected with HLA-B7, a cross-reactive allele with HLA-B27, also demonstrate a similar altered bacterial invasion phenotype. The decrease in the ability of the bacteria to penetrate the HLA-B27 and HLA-B7 transfectants is an invasion-mediated event, as demonstrated by differential invasion events using Escherichia coli transfected with the inv gene of Yersinia enterocolitica. The lysine at position 70, although unique to the HLA-B27 subtypes, is shown to be not involved in mediating the decrease in invasion. However, the ME1 epitope is the critical factor in determining allele-specific alteration in invasion on the basis of the following: 1) ME1 mAb preincubation reverses the decrease; 2) ME1-binding alleles act like HLA-B27; 3) a class I allele that is intermediate in ME1 binding (HLA-B14) also demonstrates a relative decrease in invasion; and 4) mutation at residue 67 (C-->Y) in HLA-B27, which eliminates the ME1 epitope, normalizes the decreased invasion seen in the native HLA-B27-transfected cells. Thus, the ME1 epitope relates to the disease susceptibility for reactive arthritis that is conferred by both HLA-B27 and cross-reactive group Ags.
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PMID:ME1 epitope of HLA-B27 confers class I-mediated modulation of gram-negative bacterial invasion. 751 24

Aim of this paper is to discuss, on the basis of an extensive critical review of the recent literature, the case of a 56-yr-old male patient who suffered from cutaneous psoriasis and psoriatic arthritis mutilans (PA) (polyarticular, symmetric, destruent and erosive) with involvement of the hands, feet and spine, associated with android obesity and mild type 2 diabetes mellitus. HLA typing of the patient showed the HLA-A3-Ax, B14-B63 and Cw4-Cw6 haplotypes, some of which are associated or correlated with susceptibility to PA. Cutaneous psoriasis is a chronic inflammatory dermatitis, with onset at any age and affecting approximately 2% of the western populations. In 5-7% of patients, it is associated with articular manifestations or true arthritis. PA is a chronic, inflammatory, seronegative arthropathy which may develop in some psoriasis patients, may involve peripheral and axial (spondarthritis) joints and may lead to severe joint destruction. Genetic, immunologic and environmental (i.e., infectious agents or trauma) factors seem to play an important role in the onset and clinical appearance of PA. Although PA is a clinically monomorphic disease, it may show different heterogenous subgroups with differences in their etiopathogenesis. When PA is suspected, it is mandatory to analyze carefully the patient's familiar history, search attentively for the specific skin features, exclude a septic arthritis (especially if the involvement is monoarticular) and, in the cases of fulminant disease, consider always the possible coexistence of an acquired immunodeficiency syndrome. PA can occasionally be an aggressive, disfigurating and disabling disease and the treatment (incisive and precocious) should be similar to that for rheumatoid arthritis. At present, a definitive therapy does not yet exist, but the majority of PA patients can lead a fairly normal life and they do not show increased mortality rates (excluding the severe cases of erythrodermic or pustulosis psoriasis). However, as a result of the various problems of occupation and morbidity it causes, PA is a disease with great social involvement.
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PMID:[Psoriasis complicated with severe mutilating psoriatic osteoarthropathy. Clinical case and review of the literature]. 1122 Feb 3

There is a strong association between seronegative arthritis and HLA B27, but it is still unresolved whether the contribution of B27 to disease pathogenesis is solely as a restriction element for an arthritogenic peptide, or whether B27 itself serves as an autoantigen. This study uses transgenic rats to address the question as to whether exposure to an arthritogenic pathogen can alter tolerance to B27. Unlike their nontransgenic counterparts, B27-transgenic rats are tolerant of B27 immunization using either B27(+) splenocytes or plasmid DNA and do not develop anti-B27 CTL. However, if splenocytes from such immunized animals are exposed to Chlamydia in vitro, CTL are generated that lyse B27(+) targets. No killing was seen with targets transfected with control B7, B14, B40, or B44. This phenomenon was not observed with immunization by nontransgenic splenocytes, or HLA-A2 DNA alone. Using targets expressing mutated B27, we show that the epitope for autoreactive CTL recognition of B27 involves the Lys(70) amino acid residue in the alpha(1) domain of the MHC class I molecule. The generation of CTL with specificity for B27 under these conditions demonstrates that tolerance to B27 can be subverted by CHLAMYDIA: This indicates a dynamic interrelationship between the pathogen and B27, which may have important implications for B27-related spondyloarthropathies triggered by intracellular bacteria.
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PMID:Breakdown of CTL tolerance to self HLA-B*2705 induced by exposure to Chlamydia trachomatis. 1224 6

The peptide specificity of HLA-B*1403, an allotype associated with ankylosing spondylitis (Lopez-Larrea, C., Mijiyawa, M., Gonzalez, S., Fernandez-Morera, J. L., Blanco-Gelaz, M. A., Martinez-Borra, J., and Lopez-Vazquez, A. (2002) Arthritis Rheum. 46, 2968-2971) was compared with those of the non-associated B*1402 and the prototypic disease-associated B*2705 allotypes. Although differing by a single residue (L156R), B*1402 and B*1403 shared only 32-35% of their peptide repertoires. Subtype-related differences observed in multiple peptide positions, including P3 and P7, were largely explained by a direct effect of the L156R change on peptide specificity. The HLA-B14 subtypes shared only approximately 3% of their peptide repertoires with B*2705. This was due to distinct residue usage at most positions, as revealed by statistical comparison of B*1402, B*1403, and B*2705-bound nonamers. Nevertheless, shared ligands between B*2705 and B*1403 were formally identified, although ligands common to B*2705 and B*1403, but absent from B*1402, were not found. Alloreactive T-cells were used as a tool to analyze epitope sharing among B*1402, B*1403, and B*2705. The percentage of cross-reactive T-cell clones closely paralleled peptide overlap, suggesting that shared ligands tend to maintain their antigenic features when bound to the different allotypes. Our results indicate that B*1403 and B*2705 can present common peptides. However, both the disparity of their peptide repertoires and the lack of binding features shared by these two allotypes, but not B*1402, argue against, although do not exclude, a mechanism of spondyloarthritis mediated by specific ligands of B*2705 and B*1403.
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PMID:Two HLA-B14 subtypes (B*1402 and B*1403) differentially associated with ankylosing spondylitis differ substantially in peptide specificity but have limited peptide and T-cell epitope sharing with HLA-B27. 1611 62