Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0027121 (myositis)
 4,538 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Recent studies have shown an up-regulation of the Fas/Fas ligand system in inflammatory myopathies. In myositis, however, the major Fas-mediated cytotoxicity which activates caspases bypasses apoptosis. We therefore evaluated the expression of proteins promoting cell survival, such as bcl-2, bcl-x(l) and cyclin-dependent kinase inhibitors, on muscle biopsies from 14 patients with polymyositis, dermatomyositis, inclusion body myositis and HIV-associated myositis. Our data demonstrate that inflammatory cells are immunoreactive for bcl-x(l), p16 and p57, three apoptosis-preventing proteins. Hence, we assume that these proteins might protect T cells from apoptotic nuclear changes. Our results could explain the non-self-limiting nature of inflammatory myopathies.
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PMID:T-cell anti-apoptotic mechanisms in inflammatory myopathies. 1106 32

The myositides are systemic autoimmune conditions of which the most important are polymyositis, dermatomyositis, and inclusion body myositis. In addition to the classic clinical diagnostic criteria, myositis-specific autoantibodies were identified about 15 years ago. Among the dozen or so myositis-specific autoantibodies reported to date, the most characteristic are directed against cytoplasmic antigens, such as tRNA synthetase (Jo-1 or PL-1, PL-7, PL-12, EJ, OJ, JS, and KS), signal-recognition particle (SRP), Mas, KJ, Fer (eEF1), and Wa. Antibodies to nuclear antigens include anti-Mi-2, anti-PMS (PMS1, and PMS2), and related antibodies (MLH1, DNA protein kinase catalytic subunit (DNA PKCS)...), and anti-56 kDa. Myositis-associated antibodies are not specific but may be found in patients with myositis. They are directed to nuclear or nucleolar antigens such as PM-Scl, Ku, RNP (U1-RNP and U2-RNP, U4/U6-RNP, and U5-RNP), Ro 52 kDa and, more rarely, Ro 60 kDa and La. Myositis-specific antibodies have proved useful on two fronts. They have improved the diagnosis of myositis by leading to the identification of characteristic clinical patterns, such as anti-synthetase syndrome. The place of autoantibodies alongside classic clinical and laboratory criteria remains to be determined, however. First, standardized assays will have to be developed to replace current detection methods, which use widely variable techniques and antigen preparations. Myositis-specific antibodies have also shed light on the pathogenesis of myositis. For instance, the development of antibodies to tRNA synthetases constitutes an original autoimmunity model that shows how muscle damage, probably of a nonspecific nature, can lead to the production of autoantibodies that perpetuate and aggravate the muscle lesions.
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PMID:Contribution of autoantibodies to the diagnosis and nosology of inflammatory muscle disease. 1711 Jan 50