Autoinflammation: translating mechanism to therapy
Identifieur interne : 004856 ( Pmc/Curation ); précédent : 004855; suivant : 004857Autoinflammation: translating mechanism to therapy
Auteurs : Taylor A. Doherty ; Susannah D. Brydges [États-Unis] ; Hal M. Hoffman [États-Unis]Source :
- Journal of Leukocyte Biology [ 0741-5400 ] ; 2011.
Abstract
Review discusses autoinflammatory diseases as a new classification of immune disorders due to dysregulated innate immunity yet sensitive to targeted cytokine therapy.
Url:
DOI: 10.1189/jlb.1110616
PubMed: 21330349
PubMed Central: 3219035
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<front><journal-meta><journal-id journal-id-type="nlm-ta">J Leukoc Biol</journal-id><journal-id journal-id-type="hwp">jleub</journal-id><journal-id journal-id-type="pmc">jleub</journal-id><journal-id journal-id-type="publisher-id">JLB</journal-id><journal-title-group><journal-title>Journal of Leukocyte Biology</journal-title></journal-title-group><issn pub-type="ppub">0741-5400</issn><issn pub-type="epub">1938-3673</issn><publisher><publisher-name>Society for Leukocyte Biology</publisher-name><publisher-loc>Bethesda, MD, USA</publisher-loc></publisher></journal-meta><article-meta><article-id pub-id-type="pmid">21330349</article-id><article-id pub-id-type="pmc">3219035</article-id><article-id pub-id-type="publisher-id">3RI1110-616</article-id><article-id pub-id-type="doi">10.1189/jlb.1110616</article-id><article-categories><subj-group subj-group-type="heading"><subject>Reviews</subject></subj-group></article-categories><title-group><article-title>Autoinflammation: translating mechanism to therapy</article-title></title-group><contrib-group><contrib contrib-type="author"><name><surname>Doherty</surname><given-names>Taylor A.</given-names></name><xref ref-type="aff" rid="aff1">*</xref></contrib><contrib contrib-type="author"><name><surname>Brydges</surname><given-names>Susannah D.</given-names></name><xref ref-type="aff" rid="aff2"><sup>†</sup></xref></contrib><contrib contrib-type="author"><name><surname>Hoffman</surname><given-names>Hal M.</given-names></name><xref ref-type="aff" rid="aff1">*</xref><xref ref-type="aff" rid="aff2"><sup>†</sup></xref><xref ref-type="corresp" rid="cor1"><sup>1</sup></xref></contrib><aff id="aff1">Departments of<label>*</label>Medicine and</aff><aff id="aff2"><label>†</label>Pediatrics, Division of Allergy, Immunology, and Rheumatology, University of California at San Diego and Rady Children's Hospital, La Jolla, CA, USA</aff></contrib-group><author-notes><corresp id="cor1"><label>1.</label>Correspondence: <addr-line>Departments of Medicine and Pediatrics, Division of Allergy, Immunology, and Rheumatology, University of California at San Diego, School of Medicine, 9500 Gilman Dr., La Jolla, CA 92093-0635, USA.</addr-line> E-mail: <email>hahoffman@ucsd.edu</email></corresp></author-notes><pub-date pub-type="ppub"><month>7</month><year>2011</year></pub-date><pub-date pub-type="pmc-release"><day>1</day><month>7</month><year>2012</year></pub-date><pmc-comment> PMC Release delay is 12 months and 0 days and was based on the
<volume>90</volume><issue>1</issue><fpage>37</fpage><lpage>47</lpage><history><date date-type="received"><day>15</day><month>11</month><year>2010</year></date><date date-type="rev-recd"><day>19</day><month>1</month><year>2011</year></date><date date-type="accepted"><day>25</day><month>1</month><year>2011</year></date></history><permissions><copyright-statement>© 2011 Society for Leukocyte Biology</copyright-statement><copyright-year>2011</copyright-year></permissions><self-uri xlink:title="pdf" xlink:type="simple" xlink:href="zgb00711000037.pdf"></self-uri><abstract abstract-type="precis"><p>Review discusses autoinflammatory diseases as a new classification of immune disorders due to dysregulated innate immunity yet sensitive to targeted cytokine therapy.</p></abstract><abstract><p>Autoinflammatory syndromes are a clinically heterogeneous collection of diseases characterized by dysregulation of the innate immune system. The hereditary recurrent fever disorders were the first to be defined as autoinflammatory. Several of the responsible genes are now known to encode proteins forming multimeric complexes called inflammasomes, which are intracellular “danger sensors” that respond to a variety of different signals by activating caspase-1, responsible for cleavage and subsequent release of bioactive IL-1β. This discovery of the causative link between autoinflammation and IL-1β maturation has led to a significantly improved understanding of the mechanisms of innate immunity, as well as life-altering treatments for patients. Targeting IL-1β for the treatment of autoinflammatory syndromes is an excellent example of the power of translational research. Given the central role of inflammation in many complex multigenic diseases, these treatments may benefit larger numbers of patients in the future. Here, we review current treatment strategies of autoinflammatory diseases with a focus on IL-1 antagonism.</p></abstract><kwd-group><kwd>cryopyrin</kwd><kwd>NLRP3</kwd><kwd>interleukin-1</kwd></kwd-group></article-meta></front></pmc></record>Pour manipuler ce document sous Unix (Dilib)
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