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   <subfield code="a">10.1007/s00011-011-0324-7</subfield>
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   <subfield code="a">(NATIONALLICENCE)springer-10.1007/s00011-011-0324-7</subfield>
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   <subfield code="a">Dectin-1 and NOD2 mediate cathepsin activation in zymosan-induced arthritis in mice</subfield>
   <subfield code="h">[Elektronische Daten]</subfield>
   <subfield code="c">[Holly Rosenzweig, Jenna Clowers, Gabriel Nunez, James Rosenbaum, Michael Davey]</subfield>
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   <subfield code="a">Objective: Activation of pattern recognition receptors (PRR) may contribute to arthritis. Here, we elucidated the role of NOD2, a genetic cause of inflammatory arthritis, and several other PRR in a murine model of inflammatory arthritis. Methods: The roles of CR3, TLR2, MyD88, NOD1, NOD2, Dectin-1 and Dectin-2 were tested in vivo in arthritis elicited by intra-articular injections of zymosan, the fungal cell wall components curdlan, laminarin and mannan, and the bacterial cell wall peptidoglycan. Results: Dectin-1, and to a lesser extent Dectin-2, contributed to arthritis. TLR2, MyD88 and CR3 played non-essential roles. Observations based on injection of curdlan, laminarin or mannan supported the dominant role of the Dectin-1 pathway in the joint. We demonstrated differential roles for NOD1 and NOD2 and identified NOD2 as a novel and essential mediator of zymosan-induced arthritis. Conclusions: Together, Dectin-1 and NOD2 are critical, sentinel receptors in the arthritogenic effects of zymosan. Our data identify a novel role for NOD2 during inflammatory responses within joints.</subfield>
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   <subfield code="a">Springer Basel AG, 2011</subfield>
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  <datafield tag="690" ind1=" " ind2="7">
   <subfield code="a">Arthritis models</subfield>
   <subfield code="2">nationallicence</subfield>
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  <datafield tag="690" ind1=" " ind2="7">
   <subfield code="a">NOD2</subfield>
   <subfield code="2">nationallicence</subfield>
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  <datafield tag="690" ind1=" " ind2="7">
   <subfield code="a">In vivo inflammation</subfield>
   <subfield code="2">nationallicence</subfield>
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  <datafield tag="690" ind1=" " ind2="7">
   <subfield code="a">Innate immunity</subfield>
   <subfield code="2">nationallicence</subfield>
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  <datafield tag="690" ind1=" " ind2="7">
   <subfield code="a">Zymosan</subfield>
   <subfield code="2">nationallicence</subfield>
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   <subfield code="a">Rosenzweig</subfield>
   <subfield code="D">Holly</subfield>
   <subfield code="u">Oregon Health and Science University, Mail stop: L467 AD, 3181 SW Sam Jackson Park Rd, 97239, Portland, OR, USA</subfield>
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   <subfield code="a">Clowers</subfield>
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   <subfield code="u">Oregon Health and Science University, Mail stop: L467 AD, 3181 SW Sam Jackson Park Rd, 97239, Portland, OR, USA</subfield>
   <subfield code="4">aut</subfield>
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   <subfield code="a">Nunez</subfield>
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   <subfield code="u">University of Michigan Medical School, Ann Arbor, MI, USA</subfield>
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   <subfield code="a">Rosenbaum</subfield>
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   <subfield code="u">Oregon Health and Science University, Mail stop: L467 AD, 3181 SW Sam Jackson Park Rd, 97239, Portland, OR, USA</subfield>
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   <subfield code="a">Davey</subfield>
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   <subfield code="u">Oregon Health and Science University, Mail stop: L467 AD, 3181 SW Sam Jackson Park Rd, 97239, Portland, OR, USA</subfield>
   <subfield code="4">aut</subfield>
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   <subfield code="t">Inflammation Research</subfield>
   <subfield code="d">SP Birkhäuser Verlag Basel</subfield>
   <subfield code="g">60/7(2011-07-01), 705-714</subfield>
   <subfield code="x">1023-3830</subfield>
   <subfield code="q">60:7&lt;705</subfield>
   <subfield code="1">2011</subfield>
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   <subfield code="z">Onlinezugriff via DOI</subfield>
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   <subfield code="a">Metadata rights reserved</subfield>
   <subfield code="b">Springer special CC-BY-NC licence</subfield>
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