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<record><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en">Infection in systemic lupus erythematosus: friend or foe?</title><author><name sortKey="Francis, Lisa" sort="Francis, Lisa" uniqKey="Francis L" first="Lisa" last="Francis">Lisa Francis</name></author><author><name sortKey="Perl, Andras" sort="Perl, Andras" uniqKey="Perl A" first="Andras" last="Perl">Andras Perl</name></author></titleStmt><publicationStmt><idno type="wicri:source">PMC</idno><idno type="pmid">20209114</idno><idno type="pmc">2830655</idno><idno type="url">http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2830655</idno><idno type="RBID">PMC:2830655</idno><idno type="doi">10.2217/ijr.09.72</idno><date when="2010">2010</date><idno type="wicri:Area/Pmc/Corpus">000372</idno><idno type="wicri:explorRef" wicri:stream="Pmc" wicri:step="Corpus" wicri:corpus="PMC">000372</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en" level="a" type="main">Infection in systemic lupus erythematosus: friend or foe?</title><author><name sortKey="Francis, Lisa" sort="Francis, Lisa" uniqKey="Francis L" first="Lisa" last="Francis">Lisa Francis</name></author><author><name sortKey="Perl, Andras" sort="Perl, Andras" uniqKey="Perl A" first="Andras" last="Perl">Andras Perl</name></author></analytic><series><title level="j">International journal of clinical rheumatology</title><idno type="ISSN">1758-4272</idno><idno type="eISSN">1758-4280</idno><imprint><date when="2010">2010</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en"><p id="P1">Infectious agents have long been implicated in the pathogenesis of systemic lupus erythematosus. Common viruses, such as the Epstein-Barr virus, transfusion transmitted virus, parvovirus and cytomegalovirus, have an increased prevalence in patients with systemic lupus erythematosus. They may contribute to disease pathogenesis through triggering autoimmunity via structural or functional molecular mimicry, encoding proteins that induce cross-reactive immune responses to self antigens or modulate antigen processing, activation, or apoptosis of B and T cells, macrophages or dendritic cells. Alternatively, some infectious agents, such as malaria, <italic>Toxoplasma gondii</italic> and <italic>Helicobacter pylori,</italic> may have a protective effect. Vaccinations may play dual roles by protecting against friend and foe alike.</p></div></front></TEI><pmc article-type="research-article" xml:lang="EN"><pmc-comment>The publisher of this article does not allow downloading of the full text in XML form.</pmc-comment>
<pmc-dir>properties manuscript</pmc-dir>
<front><journal-meta><journal-id journal-id-type="nlm-journal-id">101503080</journal-id><journal-id journal-id-type="pubmed-jr-id">36353</journal-id><journal-id journal-id-type="nlm-ta">Int J Clin Rheumtol</journal-id><journal-title>International journal of clinical rheumatology</journal-title><issn pub-type="ppub">1758-4272</issn><issn pub-type="epub">1758-4280</issn></journal-meta><article-meta><article-id pub-id-type="pmid">20209114</article-id><article-id pub-id-type="pmc">2830655</article-id><article-id pub-id-type="doi">10.2217/ijr.09.72</article-id><article-id pub-id-type="manuscript">NIHMS180331</article-id><article-categories><subj-group subj-group-type="heading"><subject>Article</subject></subj-group></article-categories><title-group><article-title>Infection in systemic lupus erythematosus: friend or foe?</article-title></title-group><contrib-group><contrib contrib-type="author"><name><surname>Francis</surname><given-names>Lisa</given-names></name></contrib><contrib contrib-type="author"><name><surname>Perl</surname><given-names>Andras</given-names></name><xref ref-type="corresp" rid="CR1">†</xref></contrib><aff id="A1">Division of Rheumatology, Department of Medicine State University of New York, College of Medicine 750 East Adams Street Syracuse, New York 13210, USA</aff></contrib-group><author-notes><corresp id="CR1"><label>†</label>Author for correspondence: Tel.: +1 315 464 4194 Fax: +1 315 464 4176 <email>perla@upstate.edu</email></corresp></author-notes><pub-date pub-type="nihms-submitted"><day>23</day><month>2</month><year>2010</year></pub-date><pub-date pub-type="ppub"><day>1</day><month>2</month><year>2010</year></pub-date><pub-date pub-type="pmc-release"><day>1</day><month>12</month><year>2010</year></pub-date><volume>5</volume><issue>1</issue><fpage>59</fpage><lpage>74</lpage><permissions><copyright-statement>© 2010 Future Medicine Ltd</copyright-statement><copyright-year>2010</copyright-year></permissions><abstract><p id="P1">Infectious agents have long been implicated in the pathogenesis of systemic lupus erythematosus. Common viruses, such as the Epstein-Barr virus, transfusion transmitted virus, parvovirus and cytomegalovirus, have an increased prevalence in patients with systemic lupus erythematosus. They may contribute to disease pathogenesis through triggering autoimmunity via structural or functional molecular mimicry, encoding proteins that induce cross-reactive immune responses to self antigens or modulate antigen processing, activation, or apoptosis of B and T cells, macrophages or dendritic cells. Alternatively, some infectious agents, such as malaria, <italic>Toxoplasma gondii</italic> and <italic>Helicobacter pylori,</italic> may have a protective effect. Vaccinations may play dual roles by protecting against friend and foe alike.</p></abstract><kwd-group><kwd>autoimmunity</kwd><kwd>infections</kwd><kwd>protective</kwd><kwd>systemic lupus erythematosus</kwd><kwd>vaccination</kwd></kwd-group><contract-num rid="AI1">R56 AI048079-06
||AI</contract-num><contract-num rid="AI1">R01 AI072648-01A2
||AI</contract-num><contract-num rid="AI1">R01 AI048079-06A2
||AI</contract-num><contract-sponsor id="AI1">National Institute of Allergy and Infectious Diseases Extramural Activities : NIAID</contract-sponsor></article-meta></front></pmc></record>Pour manipuler ce document sous Unix (Dilib)
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