Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011633 (dermatomyositis)
 4,181 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Anti-PL7 antibodies to threonyl-tRNA synthetase purified from beef liver were observed in the serum of a dermatopolymyositis patient. They were identified by CIE and DID using a standard anti-PL7 antiserum and quantified by ELISA in serum samples taken over a five year period. The level of antibodies against not only threonyl-tRNA synthetase but also several muscle proteins including tropomyosin, was strongly correlated with disease activity and treatment. This correlation may prove important both in monitoring the response of the patient to treatment and to our understanding of the aetiology of the disease.
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PMID:Polydermatomyositis with anti-PL7 antibody: clinical and laboratory follow-up over a five year period. 259 Nov 29

The prevalence and clinical correlations of anti-threonyl-transfer RNA synthetase (anti-PL-7), as well as the relationship of anti-PL-7 to anti-histidyl-transfer RNA synthetase (anti-Jo-1) were studied in 109 sera from patients with myositis. Inhibition of threonine aminoacylation was used to screen for anti-PL-7. Sera from 3 patients, 2 with polymyositis and 1 with polymyositis-overlap syndrome, and a fourth serum from a patient with dermatomyositis, which was previously found to contain anti-PL-7, inhibited greater than 90% of activity (3.7% of 109 sera). All 4 sera reacted strongly in an enzyme-linked immunosorbent assay with enzyme that was either affinity purified with anti-PL-7 or was biochemically purified. There was no indication of cross-reactivity by aminoacylation inhibition or, for most sera, by enzyme-linked immunosorbent assay. Anti-PL-7 is an uncommon myositis-associated antibody that is independent of anti-Jo-1, but is directed at a functionally related enzyme.
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PMID:Antibody to threonyl-transfer RNA synthetase in myositis sera. 312 89

We have developed an enzyme-linked immunosorbent assay (ELISA) specific for autoantibodies directed against the autoantigen Jo-1 (histidyl-tRNA synthetase) using antigen prepared biochemically from HeLa cells. No other patient sera, including those containing antibodies directed at threonyl-tRNA synthetase or alanyl-tRNA synthetase, reacted in the assay. Screening of sera from 169 patients with a variety of autoimmune and neuromuscular diseases confirmed that anti-Jo-1 antibodies are confined to a subgroup of patients with pure polymyositis, pure dermatomyositis, or myositis associated with another rheumatic disease.
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PMID:An enzyme-linked immunosorbent assay for the detection and quantitation of anti-Jo-1 antibody in human serum. 349 84

We describe a patient with dermatomyositis and inflammatory polyarthritis with erosive wrist arthropathy who was found to have the anti-PL-7 autoantibody directed against threonyl-tRNA synthetase.
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PMID:Dermatomyositis with erosive arthropathy: association with the anti-PL-7 antibody. 1060 85

Autoantibodies to histidyl-tRNA synthetase (HisRS) or to alanyl-, asparaginyl-, glycyl-, isoleucyl-, or threonyl-tRNA synthetase occur in approximately 25% of patients with polymyositis or dermatomyositis. We tested the ability of several aminoacyl-tRNA synthetases to induce leukocyte migration. HisRS induced CD4(+) and CD8(+) lymphocytes, interleukin (IL)-2-activated monocytes, and immature dendritic cells (iDCs) to migrate, but not neutrophils, mature DCs, or unstimulated monocytes. An NH(2)-terminal domain, 1-48 HisRS, was chemotactic for lymphocytes and activated monocytes, whereas a deletion mutant, HisRS-M, was inactive. HisRS selectively activated CC chemokine receptor (CCR)5-transfected HEK-293 cells, inducing migration by interacting with extracellular domain three. Furthermore, monoclonal anti-CCR5 blocked HisRS-induced chemotaxis and conversely, HisRS blocked anti-CCR5 binding. Asparaginyl-tRNA synthetase induced migration of lymphocytes, activated monocytes, iDCs, and CCR3-transfected HEK-293 cells. Seryl-tRNA synthetase induced migration of CCR3-transfected cells but not iDCs. Nonautoantigenic aspartyl-tRNA and lysyl-tRNA synthetases were not chemotactic. Thus, autoantigenic aminoacyl-tRNA synthetases, perhaps liberated from damaged muscle cells, may perpetuate the development of myositis by recruiting mononuclear cells that induce innate and adaptive immune responses. Therefore, the selection of a self-molecule as a target for an autoantibody response may be a consequence of the proinflammatory properties of the molecule itself.
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PMID:Histidyl-tRNA synthetase and asparaginyl-tRNA synthetase, autoantigens in myositis, activate chemokine receptors on T lymphocytes and immature dendritic cells. 1223 11

Autoantibodies against several aminoacyl-transfer-RNA synthetases have been described in patients with myositis; anti-threonyl-tRNA synthetase (anti-PL-7) is one of the rarest. We describe the clinical and laboratory characteristics of a cohort of European anti-PL-7 patients, and compare them with previously reported cases. This multicenter study of patients positive for anti-PL-7, identified between 1984 and 2011, derives from the EUMYONET cohort. Clinical and serologic data were obtained by retrospective laboratory and medical record review, and statistical analyses were performed with chi-squared and Fisher exact tests. Eighteen patients, 15 women, were anti-PL-7 antibody positive. Median follow-up was 5.25 years (interquartile range, 2.8-10.7 yr), and 4 patients died. All patients had myositis (12 polymyositis, 5 dermatomyositis, and 1 amyopathic dermatomyositis), 10 (55.6%) had interstitial lung disease, and 9 (50%) had pericardial effusion. Occupational exposure to organic/inorganic particles was more frequent in patients with interstitial lung disease than in the remaining patients (5 of 10 vs. 1 of 7; p = 0.152), although the difference was not significant. Concurrent autoantibodies against Ro60 and Ro52 were seen in 8 of 14 (57%) patients studied. In the literature review the most common manifestations of anti-PL-7 antisynthetase syndrome were interstitial lung disease (77%), myositis (75%), and arthritis (56%). As in other subsets of the antisynthetase syndrome, myositis and interstitial lung disease are common features of the anti-PL-7 antisynthetase syndrome. In addition, we can add pericarditis as a possible manifestation related to anti-PL-7 antibodies.
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PMID:Anti-PL-7 (anti-threonyl-tRNA synthetase) antisynthetase syndrome: clinical manifestations in a series of patients from a European multicenter study (EUMYONET) and review of the literature. 2273 51