Polymyositis-dermatomyositis and infections

University of Milan, Milano, Lombardy, Italy
Autoimmunity (Impact Factor: 2.71). 06/2006; 39(3):191-6. DOI: 10.1080/08916930600622348
Source: PubMed


In genetically predisposed individuals, viruses, bacteria, or parasitic infectious agents are suspected to induce autoimmunity and/or to exacerbate the disease once the self-tolerance is broken. Although direct evidence for this association is still lacking, numerous data from animal models as well as from humans support the hypothesis of a direct contribution of pathogens to the induction of several autoimmune diseases. This review focused on the possible role of infectious agents as triggers of autoimmunity in polymyositis (PM) and dermatomyositis (DM). Epidemiological studies, clinical and experimental findings that support the hypothesis of infection-induced PM and DM are summarized and discussed. In addition, immune response abnormalities and immunosuppressive medications may be responsible for the high percentage of infectious complications in PM and DM patients. In this review, the increased risk of developing infections in these patients is also underlined and published data are reported.

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    • "In this scenario, TIF1β would interact with viral proteins and the putative viral-self protein complex may trigger autoantibodies to TIF1β, similar to the induction of anti-p53 by a complex of viral simian virus 40 T protein and self p53 protein [37]. Association of virus and myositis autoantibody production has been suggested to occur by various pathways, including viral RNA interaction with aminoacyl tRNA synthetase and molecular mimicry of viral protein and autoantigens [38,39]. More recently, a target antigen of anti-CADM140 was identified as an intracellular viral RNA receptor, melanoma differentiation-associated gene 5 (MDA5) [13]. "
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    ABSTRACT: Myositis specific autoantibodies are associated with unique clinical subsets and are useful biomarkers in polymyositis/dermatomyositis (PM/DM). A 120 kD protein recognized by certain patients with DM was identified and clinical features of patients with this specificity were characterized. The 120 kD protein recognized by a prototype serum was purified and identified by mass spectrometry and immunological methods. Autoantibody to this 120 kD protein was screened in sera from 2,356 patients with various diagnoses from four countries, including 254 PM/DM, by immunoprecipitation of 35S-methionine labeled K562 cell extracts. Clinical information of patients with this specificity was collected. The 120 kD protein, which exactly comigrated with PL-12, was identified as transcription intermediary factor TIF1β (TRIM28) by mass spectrometry and validated by immunoassays. By immunofluorescence, anti-TIF1β positivity showed a fine-speckled nuclear staining pattern. Four cases of anti-TIF1β were identified; all are women, one each in a Japanese, African American, Caucasian, and Mexican individual. Three had a diagnosis of DM and one case was classified as having an undifferentiated connective tissue disease with an elevated CPK but without significant muscle symptoms. This individual also had a history of colon cancer, cervical squamous metaplasia and fibroid tumors of the uterus. Myopathy was mild in all cases and resolved without treatment in one case. The anti-TIF1β specificity was not found in other conditions. Anti-TIF1β is a new DM autoantibody associated with a mild form of myopathy. Whether it has an association with malignancy, as in the case of anti-TIF1γ, or other unique features will need to be evaluated in future studies.
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    ABSTRACT: The parasite Toxoplasma gondii mainly encysts in brain, retina, myocardium, and skeletal muscle. It has been implicated in the genesis of inflammatory myopathies for years, but the parasite usually cannot be detected in the muscle. It is established, however, that toxoplasmosis can cause myositis either by recent infection or by reactivation. The case of a non-HIV patient who developed an acute polymyositis upon infection by T. gondii is reported. We suggest that all patients with polymyositis should have serological tests for toxoplasmosis as a part of their initial evaluation and early trial of antiprotozoal therapy in case of positive findings.
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