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)

Collagen induced arthritis is an experimental animal model of inflammatory polyarthropathy that has many features of human rheumatoid arthritis. Type II collagen is the major matrix protein of hyaline cartilage and is a sequestered protein which can be presented as an autoantigen under certain conditions. To induce CIA, type II collagen is injected intradermally with complete Freund's adjuvant. Susceptibility to CIA is dependent on the presence of the trimolecular complex: 1) the arthritogenic epitope on the type II collagen; 2) a class II MHC molecule on the accessory cell presenting the arthritogenic epitope; and 3) T cells expressing specific V beta chains in their TCRs. Complement and other non-MHC background genes also may play a role in susceptibility to CIA. Both cell mediated and humoral immunity are involved in the pathogenesis of CIA. To date immunotherapies that have modulated CIA include use of anti-class Ii antibodies, anti-lymphokines, and monoclonal antibodies directed against specific cellular markers. All of these therapies are able to modulate disease to some extent but lack the specificity and efficacy to make them practical for widespread use in human disease. Most promising, is the use of monoclonal antibodies directed against specific V beta TCR subsets. This is potentially a very specific and effective therapy because it will affect only the cells involved in disease while leaving the host otherwise immunocompetent. Therapies on the horizon include the use of synthetic peptides with sequences homologous to various regions on the TCR, immunotoxins, and superantigens to modulate the immune response and ameliorate disease.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Immunogenetics of collagen induced arthritis in mice: a model for human polyarthritis. 128 54

Major conflicts in history have yielded an equal number of medical casualties as those injured in battle, and no more common a problem exists in the insanitary conditions of war as dysentery. The complication of arthritis following dysentery has been documented since ancient times, but it is not until the 16th Century that these cases appear in any numbers, and then it is predominantly in military personnel. "Reiter's Disease" is currently understood to mean an asymmetrical, predominantly lower-limb polyarthritis developing after urethritis (usually non-gonococcal) or dysentery; conjunctivitis is not always a constant feature. This is the commonest inflammatory polyarthropathy of young men and both the epidemic (dysenteric) and sporadic (venereal) forms are historically prevalent in soldiers--a not surprising fact considering the squalor of war and the unrestrained behaviour of the Private soldier. This paper traces the history of Reiter's disease and highlights its affinity for military populations.
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PMID:Reiter's disease: an historical review of a soldiers' disease. 226 34

The development of reactive arthritis, a sterile inflammatory polyarthropathy that primarily affects HLA-B27 positive individuals, has been associated with previous enteric infections caused by various gram-negative bacteria. The possibility that a common bacterial epitope triggers the disease was investigated by screening a panel of documented arthritogenic Shigella strains as well as 2 epidemic-associated nonarthritogenic Shigella controls. A 2-Md plasmid specific to the arthritogenic strains was identified and sequenced. The plasmid encodes a number of small peptides that could be related to the development of reactive arthritis. Within 1 of these is a stretch of 5 consecutive amino acids, inferred from the DNA sequence and contained within an open reading frame, that is homologous to amino acid residues 71-75 of the polymorphic region of the alpha 1 domain of HLA-B27. The data indicate that there is a bacterial plasmid common to arthritogenic Shigella strains that may play a role in triggering reactive arthritis. The finding that this plasmid encodes an epitope shared with HLA-B27 suggests that molecular mimicry may play a role in the induction of this disease.
Arthritis Rheum 1989 Aug
PMID:Identification of a 2-Md plasmid from Shigella flexneri associated with reactive arthritis. 247 14

Previously, we reported that human T cell leukemia virus type-1 env-pX region-introduced transgenic (pX-Tg) mice develop an inflammatory polyarthropathy. Although autoimmune pathogenesis was suggested, the detailed mechanisms remain to be elucidated. In this report, we examined effects of the MHC and fas genes on the development of the disease. When pX-Tg mice were backcrossed with different inbred strains, the incidence of arthritis differed among strains; 64% and 72% in BALB/cAn (H-2d), 25% and 46% in C3H/HeN (H-2k), and 0% and 2% in C57BL/6J (H-2b) background at 3 and 6 months of age, respectively. Rheumatoid factor levels in the serum correlated with the susceptibility to the disease, whereas IL-1beta and MHC gene expression were similarly elevated in all of these strains, suggesting involvement of immune regulatory genes in this strain difference. However, introduction of the H-2d locus into C57BL/6J pX-Tg mice did not increase the incidence of arthritis, and substitution of the BALB/cAn H-2 locus with the H-2b did not decrease it. The results indicate that the H-2 locus is not the major determinant of the disease. Then, since previous study indicated a defect in Fas-mediated apoptosis of transgenic T cells, the effects of fas gene modification on the disease were examined. The incidence increased when these pX-Tg mice were crossed with lpr/lpr mice, while it decreased when crossed with fas-transgenic mice. These observations suggest that aberration of Fas-mediated apoptosis of peripheral lymphocytes, rather than negative selection in the thymus, is involved in the development of autoimmune arthropathy in pX-Tg mice.
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PMID:The development of autoimmune inflammatory arthropathy in mice transgenic for the human T cell leukemia virus type-1 env-pX region is not dependent on H-2 haplotypes and modified by the expression levels of Fas antigen. 986 86

Previously, we reported that human T cell leukemia virus type I env-pX region-introduced transgenic (pX-Tg) mice developed an inflammatory polyarthropathy associated with a development of autoimmunity. To elucidate roles of autoimmunity in the development of arthritis, the immune cells were reciprocally replaced between pX-Tg mice and non-transgenic (Tg) mice. When bone marrow (BM) cells and spleen cells from pX-Tg mice were transferred into irradiated non-Tg mice, arthritis developed in these mice. In contrast, arthritis in pX-Tg mice was completely suppressed by non-Tg BM and spleen cells. Similar results were obtained with BM cells only. After the transplantation, T cells, B cells, and macrophages were replaced completely, whereas cells in the joints were replaced partially. In those mice, serum Ig and rheumatoid factor levels correlated with the disease development, and inflammatory cytokine expression was elevated in the arthritic joints. Furthermore, involvement of T cells in the joint lesion was suggested, because the incidence was greatly reduced in athymic nu/nu mice although small proportion of the mice still developed arthritis. These observations suggest that BM stem cells are abnormal, causing autoimmunity in pX-Tg mice, and this autoimmunity plays an important, but not absolute, role in the development of arthritis in this Tg mouse.
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PMID:Bone marrow-derived cells are responsible for the development of autoimmune arthritis in human T cell leukemia virus type I-transgenic mice and those of normal mice can suppress the disease. 1055 1

Case 1. A 20-year-old woman presented 4 weeks post-partum with widespread symmetrical inflammatory polyarthropathy with marked synovitis. Investigations revealed grossly raised CRP with negative immunology screen. A few days before presentation she saw her general practitioner with left-sided mastitis, which then developed into a Staphylococcus breast abscess. Surgical drainage of this led to almost immediate resolution of the joint complaints and return of CRP to normal. Case 2. A 27-year-old man developed widespread symmetrical inflammatory arthropathy. A few days prior to this he had developed folliculitis with a furuncle on his neck. Swab grew Staphylococcus aureus. His arthritis settled immediately following spontaneous drainage of his abscess and a full course of antibiotic. The pathogenic mechanism is unclear but could be toxin-mediated.
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PMID:Acute non-purulent inflammatory arthropathy associated with Staphylococcus aureus abscess. 1077 30

Between June 1991 and January 1995, 42 hydroxyapatite-coated CAD-CAM femoral components were inserted in 25 patients with inflammatory polyarthropathy, 21 of whom had juvenile idiopathic arthritis. Their mean age was 21 years (11 to 35). All the patients were reviewed clinically and radiologically at one, three and five years. At the final review at a mean of 11.2 years (8 to 13) 37 hips in 23 patients were available for assessment. A total of four femoral components (9.5%) had failed, of which two were radiologically loose and two were revised. The four failed components were in patients aged 16 years or less at the time of surgery. Hydroxyapatite-coated customized femoral components give excellent medium- to long-term results in skeletally-mature young adults with inflammatory polyarthropathy. Patients aged less than 16 years at the time of surgery have a risk of 28.5% of failure of the femoral component at approximately ten years.
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PMID:The use of hydroxyapatite-coated CAD-CAM femoral components in adolescents and young adults with inflammatory polyarthropathy: ten-year results. 1679 85