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)

This family consists of forty-eight subjects, all of whom have been examined with regard to the presence of psoriasis and nearly all for the presence of arthritic lesions (sacroiliitis and peripheral arthritis). All the members have been tissue-typed not only for HLA-A, B and C locus products but also for D locus products. This has enabled us to study the entire HLA chromosomal region. In the family concerned we have found that those subjects haploidentical with the proband have, to a very large degree, either one or all clinical manifestations, which demonstrates a close genetic relationship between joint (especially sacroiliitis) and cutaneous manifestations. These findings prompt us to repeat our previously made proposal about different phenotypic expressions of the same genotype. In this family study the disease-associated haplotypes did not contain the genes for B13, 17 or 37 antigens which are known to occur frequently in psoriatic patients. However, not all psoriasis patients have these antigens. Despite that, we believe that the gene(s) which increase the likelihood of developing psoriasis are identical in all patients and therefore family studies where the proband does not carry the particular psoriasis associated B-alleles are equally illuminating as to the inheritance pattern of disease.
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PMID:Psoriasis and arthritic lesions in relation to the inheritance of HLA genotypes: a family study. 8 75

A total of 222 female patients with seronegative rheumatic diseases were investigated by sacroiliac joint X-ray and HLA-A, B and Ctyped. The frequency of the B27 antigen was significantly increased in the following groups: definite pelvospondylitis (26 patients and relative risk (RR) = 99), possible pelvospondylitis (20 patients, RR=4.5), definite sacroiliitis (14 patients, RR-20.1) and uroarthritis (8 patients). When 24 B27 negative patients from these B27 associated diseases were analysed, significantly increased frequencies of the BW22 (RR=16.7) and CW1 (RR=14.4) antigens were found. There were no significantly deviating HLA frequencies in the following diagnostic groups: clinical sacroiliitis (20 patients), polyarthritis with clinically silent sacroiliitis (12 patients), polyarthritis without sacroiliitis (47 patients), arthralgia preceded by beta-streptococcal infection (17 patients), other arthralgia (33 patients), osteo-arthritis (13 patients) and other arthritis (12 patients).
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PMID:HLA antigens in females with ankylosing spondylitis and other forms of seronegative rheumatic diseases. 72 51

A CD8+ alpha beta TCR+ T cell clone (A35) was isolated from the synovial fluid of a patient with post-enteric reactive arthritis caused by Yersinia enterocolitica. This clone efficiently killed autologous and allogeneic target cells that had been preincubated with live but not with heat-killed bacteria. There was no restriction by polymorphic parts of HLA-A, -B, or -C molecules and a HLA class II-deficient mutant cell line was lysed as efficiently as its normal counterpart, whereas infected HLA class I-deficient cells (Daudi cells) were not. The clone showed crossreaction between Yersinia enterocolitica, Escherichia coli, Pseudomonas aeruginosa, and Streptococcus pyogenes, but did not lyse target cells preincubated with Staphylococcus epidermidis. MAb to CD2, CD3, and CD8 efficiently blocked A35, whereas the addition of mAb to HLA class II or to HLA class I did not. This clone apparently represents a novel effector mechanism against bacteria-infected or -modified cells that could be involved in the immunopathology of reactive arthritis.
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PMID:MHC-unrestricted recognition of bacteria-infected target cells by human CD8+ cytotoxic T lymphocytes. 138 47

Eighty-one patients with systemic onset juvenile chronic arthritis (JCA) have been tested for HLA-A, -B, -C, and -DR antigens. This study confirms previous reports of an increased incidence of DR4 in these patients. Subdivision of the patients according to their disease course over ten years showed different HLA associations with different disease courses. The frequency of DR4 tended to be greater in patients with less severe disease. There was also an increased incidence of HLA B27 in patients in whom relapses of disease were associated with intercurrent infections.
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PMID:Increased frequency of DR4 in systemic onset juvenile chronic arthritis. 150 14

Fourteen patients with cystic fibrosis arthritis and eight patients with cystic fibrosis and hypertrophic osteoarthropathy were typed for HLA-A, B, C, DR, and DQ antigens and were compared with age and sex matched controls with cystic fibrosis. The diagnosis of cystic fibrosis arthritis and hypertrophic osteoarthropathy was confirmed by radiography and bone scanning. The prevalence of HLA-A, B, C, D, antigens in the cystic fibrosis group (44 patients) did not differ from that in the control group. A comparison between patients with cystic fibrosis arthritis or hypertrophic osteoarthropathy and their respective controls did not show any significant differences in HLA prevalence. It is concluded that HLA antigens may not be a factor in the susceptibility of patients with cystic fibrosis to cystic fibrosis arthritis or hypertrophic osteoarthropathy.
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PMID:Absence of an association between HLA typing in cystic fibrosis arthritis and hypertrophic osteoarthropathy. 177 90

The presence of peripheral arthritis and HLA-A, B, C, DR, and DQ antigens was evaluated prospectively in 18 Caucasian men with human immunodeficiency virus-associated psoriasis. An asymmetric polyarthritis occurred in 32% of the patients and correlated with the presence of HLA-B27. Extensive clinical overlap between psoriatic arthritis, psoriasis, and Reiter's syndrome was noted. No significant excess of the HLA antigens previously found to be associated with psoriasis was seen, which suggests that human immunodeficiency virus-associated psoriasis per se may instead constitute another form of spondylarthropathy that is more closely related to Reiter's syndrome.
Arthritis Rheum 1990 Oct
PMID:Human immunodeficiency virus-associated psoriasis, psoriatic arthritis, and Reiter's syndrome: a disease continuum? 222 38

Previous studies of patients with systemic lupus erythematosus (SLE) have shown an increased frequency of certain major histocompatibility complex (MHC) markers, including HLA-DR2, DR3, and C4AQ0 (C4A-null), in Caucasian patients. However, most of these studies were of randomly selected, unrelated patients; families were not included, and haplotypes were not determined. In order to define more accurately the possible role of MHC genes in lupus susceptibility, HLA-A, B, C, and DR, as well as BF, C2, C4A, C4B, and GLO, markers were determined in 62 Caucasian patients of known ethnic background, and in the members of their families. The distributions of extended haplotypes (fixed combinations of HLA-B, DR, and complotype alleles), fragments thereof, and individual alleles were determined in SLE patients and controls. The MHC distributions in all patients were compared with haplotypes in a normal Caucasian population. There were no statistically significant differences between the frequencies of any MHC marker, fragment, or extended haplotype in the patients compared with the controls. The patients were categorized into 2 groups of European ancestry (English/Irish; other Europeans), and each group was compared with a group of ethnically matched controls. There was a statistically significantly increased frequency of the alleles C4AQ0 and DR3 and the complotype SC01 in SLE patients of English/Irish descent as compared with ethnically matched controls. The increase in C4AQ0 and DR3 could be accounted for by the fact that they were part of the extended haplotype [HLA-B8;SC01;DR3] and/or its fragment (SC01;DR3). No increase in any MHC marker was observed in the other patients.(ABSTRACT TRUNCATED AT 250 WORDS)
Arthritis Rheum 1990 Jul
PMID:The effect of ethnicity on major histocompatibility complex complement allotypes and extended haplotypes in patients with systemic lupus erythematosus. 236 33

The prevalence of HLA-A and B antigen loci in patients with Whipple's disease was determined from data obtained in a review of the literature and from personal communications. Data on the HLA-A and B locus typing of 30 patients were available (with the exception that 1 of the patients was not typed for the HLA-B locus), and for an additional 18 patients, HLA-B27 data were available. Of the 47 patients typed for B27, 13 (28%) were B27 positive. Twelve of the 48 patients had sacroiliitis, and 2 (17%) of them were B27 positive. These data suggest that Whipple's disease may be associated with HLA-B27, even in the absence of concomitant sacroiliitis.
Arthritis Rheum 1987 Jan
PMID:HLA antigens in Whipple's disease. 243 4

The strongest reported association between a class I HLA allele and disease is that of HLA-B27 with ankylosing spondylitis (AS). However, it has not been shown whether B27 is the gene that predisposes to the development of AS or if it is merely linked with the disease-susceptibility locus. Furthermore, if B27 itself is the disease-susceptibility gene, there may be epistatic loci that also contribute to the development of AS or modify its clinical manifestation. A class I HLA 9.2-kb Pvu II restriction fragment was recently identified, which, when present in a B27-positive individual, further increased the relative risk for developing AS (from 119 to 297). This study was therefore designed to confirm the association between AS and this restriction fragment length polymorphism (RFLP) and to map the location of this fragment in the genome. The data presented here suggest that the class I HLA 9.2-kb Pvu II RFLP represents a Pvu II polymorphism at the 5' end of the HLA-A locus that is tightly linked with both HLA-A3 and A9 alleles. However, there is no association between this RFLP and AS in a population of patients living in Baltimore.
Arthritis Rheum 1989 Jul
PMID:Characterization of the class I HLA 9.2-kb PVU II restriction fragment length polymorphism. Linkage to HLA-A and lack of disease association. 256 35

T lymphocytes from a patient with Shigella flexneri dysentery and postdysenteric reactive arthritis were cloned by limiting dilution with recombinant interleukin-2 and a strain of S. flexneri different from that which had infected her. Five of eight clones produced proliferated in response to the shigellae used to generate the clones. The response required irradiated syngeneic blood mononuclear cells as antigen-presenting cells. One such clone, MC12, proliferated in response to both the shigellae used to generate the clones and the infecting shigellae but not to other shigellae, Salmonella heidelberg, or control Escherichia coli. MC12 was CD3+, CD4+, CD8-, and human histocompatibility leukocyte antigen (HLA)-DR+. The proliferative response to the shigellae was blocked by antibody to HLA-DR but not by antibody to HLA-A,B,C. The response required antigen-presenting cells that shared HLA-DR antigens with the clone and appeared to be restricted by HLA-DR2. The epitope recognized by MC12 was associated with the bacterial membranes. Thus, T-lymphocyte clones that proliferate in response to some shigellae can be isolated from patients with shigellosis.
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PMID:T-lymphocyte clones responsive to Shigella flexneri. 265 77


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