<?xml version="1.0" encoding="UTF-8"?>
<?xml-stylesheet type="text/xsl" media="screen" href="/~d/styles/rss1full.xsl"?><?xml-stylesheet type="text/css" media="screen" href="http://feeds.nature.com/~d/styles/itemcontent.css"?><rdf:RDF xmlns:rdf="http://www.w3.org/1999/02/22-rdf-syntax-ns#" xmlns:prism="http://prismstandard.org/namespaces/basic/2.0/" xmlns:dc="http://purl.org/dc/elements/1.1/" xmlns:content="http://purl.org/rss/1.0/modules/content/" xmlns="http://purl.org/rss/1.0/" xmlns:admin="http://webns.net/mvcb/" xmlns:feedburner="http://rssnamespace.org/feedburner/ext/1.0">
<channel rdf:about="http://www.nature.com/ni/current_issue/rss">
<title>Nature Immunology - AOP - nature.com science feeds</title>
<description>Nature Immunology is a multidisciplinary journal that publishes papers of the highest quality and significance in all areas of immunology. Priority is given to work that provides fundamental insight into the workings of the immune system. Areas covered include, but are not limited to, innate immunity and inflammation; development; immune receptors, signaling and apoptosis; antigen presentation; gene regulation and recombination; cellular and systemic immunity; vaccines; immune tolerance; autoimmunity and tumor immunology, microbial immunopathology; and transplantation.</description>
<link>http://www.nature.com/ni/current_issue/</link>
<admin:generatorAgent rdf:resource="http://www.nature.com/" />
<admin:errorReportsTo rdf:resource="mailto:feedback@nature.com" />
<dc:publisher>Nature Publishing Group</dc:publisher>
<dc:language>en</dc:language>
<dc:rights>©  Nature Publishing Group</dc:rights>
<prism:publicationName>Nature Immunology</prism:publicationName>
<prism:issn>1529-2908</prism:issn>
<prism:eIssn>1529-2916</prism:eIssn>
<prism:copyright>©  Nature Publishing Group</prism:copyright>
<prism:rightsAgent>permissions@nature.com</prism:rightsAgent>
<image rdf:resource="http://www.nature.com/includes/rj_globnavimages/ni_logo.gif" />
<items>
<rdf:Seq>
<rdf:li rdf:resource="http://dx.doi.org/10.1038/ni.1826" />
<rdf:li rdf:resource="http://dx.doi.org/10.1038/ni.1824" />
<rdf:li rdf:resource="http://dx.doi.org/10.1038/ni.1823" />
<rdf:li rdf:resource="http://dx.doi.org/10.1038/ni.1819" />
<rdf:li rdf:resource="http://dx.doi.org/10.1038/ni.1825" />
</rdf:Seq>
</items>
<atom10:link xmlns:atom10="http://www.w3.org/2005/Atom" rel="self" href="http://feeds.nature.com/ni/rss/aop" type="application/rss+xml" /><atom10:link xmlns:atom10="http://www.w3.org/2005/Atom" rel="hub" href="http://pubsubhubbub.appspot.com" /></channel>
<image rdf:about="http://www.nature.com/includes/rj_globnavimages/ni_logo.gif">
<title>Nature Immunology</title>
<url>http://www.nature.com/includes/rj_globnavimages/ni_logo.gif</url>
<link>http://www.nature.com/ni/</link>
</image>
<item rdf:about="http://dx.doi.org/10.1038/ni.1826">
<title>Different routes of bacterial infection induce long-lived TH1 memory cells and short-lived TH17 cells</title>
<link>http://feeds.nature.com/~r/ni/rss/aop/~3/FhB9FN9i0Gc/ni.1826</link>
<description>Naive CD4+ T cells can differentiate into distinct polarized effector cells, but detailed characterization of physiologic CD4 memory is lacking. Jenkins and colleagues show that TH1 and TH17 memory cells differ in longevity and arise via different infection routes.</description>
<content:encoded><![CDATA[
<div><a href="http://ad.doubleclick.net/adj/ni.nature.com/rss;sz=728x90"><img src="http://ad.doubleclick.net/ad/ni.nature.com/rss;sz=728x90" alt="Advertisement" style="border:0" /></a></div>
<p>
<b>Different routes of bacterial infection induce long-lived TH1 memory cells and short-lived TH17 cells</b>
</p>
<p>Nature Immunology. <a href="http://dx.doi.org/10.1038/ni.1826">doi:10.1038/ni.1826</a>
</p>
<p>Authors: Marion Pepper, Jonathan L Linehan, Antonio J Pag&#225;n, Traci Zell, Thamotharampillai Dileepan, P Patrick Cleary &amp; Marc K Jenkins</p>
<img src="http://feeds.feedburner.com/~r/ni/rss/aop/~4/FhB9FN9i0Gc" height="1" width="1"/>]]></content:encoded>
<dc:title>Different routes of bacterial infection induce long-lived TH1 memory cells and short-lived TH17 cells</dc:title>
<dc:creator>Marion Pepper</dc:creator>
<dc:creator>Jonathan L Linehan</dc:creator>
<dc:creator>Antonio J Pagán</dc:creator>
<dc:creator>Traci Zell</dc:creator>
<dc:creator>Thamotharampillai Dileepan</dc:creator>
<dc:creator>P Patrick Cleary</dc:creator>
<dc:creator>Marc K Jenkins</dc:creator>
<dc:identifier>doi:10.1038/ni.1826</dc:identifier>
<dc:source>Nature Immunology</dc:source>
<dc:date>2009-11-22</dc:date>
<prism:publicationName>Nature Immunology</prism:publicationName>
<prism:publicationDate>2009-11-22</prism:publicationDate>
<prism:doi>10.1038/ni.1826</prism:doi>
<prism:url>http://dx.doi.org/10.1038/ni.1826</prism:url>
<prism:section>Article</prism:section>
<prism:startingPage />
<prism:endingPage />
<feedburner:origLink>http://dx.doi.org/10.1038/ni.1826</feedburner:origLink></item>
<item rdf:about="http://dx.doi.org/10.1038/ni.1824">
<title>Recognition of RNA virus by RIG-I results in activation of CARD9 and inflammasome signaling for interleukin 1β production</title>
<link>http://feeds.nature.com/~r/ni/rss/aop/~3/qFcOK6Mi0tk/ni.1824</link>
<description>Production of mature interleukin 1β (IL-1β) requires Il1b transcription and inflammasome-mediated processing of IL-1β protein. Ruland and colleagues show that the RNA virus sensor RIG-I signals via the adaptors CARD9 and Asc to facilitate both processes.</description>
<content:encoded><![CDATA[
<div><a href="http://ad.doubleclick.net/adj/ni.nature.com/rss;sz=728x90"><img src="http://ad.doubleclick.net/ad/ni.nature.com/rss;sz=728x90" alt="Advertisement" style="border:0" /></a></div>
<p>
<b>Recognition of RNA virus by RIG-I results in activation of CARD9 and inflammasome signaling for interleukin 1&#946; production</b>
</p>
<p>Nature Immunology. <a href="http://dx.doi.org/10.1038/ni.1824">doi:10.1038/ni.1824</a>
</p>
<p>Authors: Hendrik Poeck, Michael Bscheider, Olaf Gross, Katrin Finger, Susanne Roth, Manuele Rebsamen, Nicole Hannesschl&#228;ger, Martin Schlee, Simon Rothenfusser, Winfried Barchet, Hiroki Kato, Shizuo Akira, Satoshi Inoue, Stefan Endres, Christian Peschel, Gunther Hartmann, Veit Hornung &amp; J&#252;rgen Ruland</p>
<img src="http://feeds.feedburner.com/~r/ni/rss/aop/~4/qFcOK6Mi0tk" height="1" width="1"/>]]></content:encoded>
<dc:title>Recognition of RNA virus by RIG-I results in activation of CARD9 and inflammasome signaling for interleukin 1β production</dc:title>
<dc:creator>Hendrik Poeck</dc:creator>
<dc:creator>Michael Bscheider</dc:creator>
<dc:creator>Olaf Gross</dc:creator>
<dc:creator>Katrin Finger</dc:creator>
<dc:creator>Susanne Roth</dc:creator>
<dc:creator>Manuele Rebsamen</dc:creator>
<dc:creator>Nicole Hannesschläger</dc:creator>
<dc:creator>Martin Schlee</dc:creator>
<dc:creator>Simon Rothenfusser</dc:creator>
<dc:creator>Winfried Barchet</dc:creator>
<dc:creator>Hiroki Kato</dc:creator>
<dc:creator>Shizuo Akira</dc:creator>
<dc:creator>Satoshi Inoue</dc:creator>
<dc:creator>Stefan Endres</dc:creator>
<dc:creator>Christian Peschel</dc:creator>
<dc:creator>Gunther Hartmann</dc:creator>
<dc:creator>Veit Hornung</dc:creator>
<dc:creator>Jürgen Ruland</dc:creator>
<dc:identifier>doi:10.1038/ni.1824</dc:identifier>
<dc:source>Nature Immunology</dc:source>
<dc:date>2009-11-15</dc:date>
<prism:publicationName>Nature Immunology</prism:publicationName>
<prism:publicationDate>2009-11-15</prism:publicationDate>
<prism:doi>10.1038/ni.1824</prism:doi>
<prism:url>http://dx.doi.org/10.1038/ni.1824</prism:url>
<prism:section>Article</prism:section>
<prism:startingPage />
<prism:endingPage />
<feedburner:origLink>http://dx.doi.org/10.1038/ni.1824</feedburner:origLink></item>
<item rdf:about="http://dx.doi.org/10.1038/ni.1823">
<title>Nod1 and Nod2 direct autophagy by recruiting ATG16L1 to the plasma membrane at the site of bacterial entry</title>
<link>http://feeds.nature.com/~r/ni/rss/aop/~3/0B5CognjkQQ/ni.1823</link>
<description>Autophagy facilitates host defense against invading bacteria. Philpott and colleagues show that Nod1 and Nod2 link pathogen sensing to autophagy by recruiting the autophagy protein AGT16L1 to the site of pathogen entry.</description>
<content:encoded><![CDATA[
<div><a href="http://ad.doubleclick.net/adj/ni.nature.com/rss;sz=728x90"><img src="http://ad.doubleclick.net/ad/ni.nature.com/rss;sz=728x90" alt="Advertisement" style="border:0" /></a></div>
<p>
<b>Nod1 and Nod2 direct autophagy by recruiting ATG16L1 to the plasma membrane at the site of bacterial entry</b>
</p>
<p>Nature Immunology. <a href="http://dx.doi.org/10.1038/ni.1823">doi:10.1038/ni.1823</a>
</p>
<p>Authors: Leonardo H Travassos, Leticia A M Carneiro, Mahendrasingh Ramjeet, Seamus Hussey, Yun-Gi Kim, Jo&#227;o G Magalh&#227;es, Linda Yuan, Fraser Soares, Evelyn Chea, Lionel Le Bourhis, Ivo G Boneca, Abdelmounaaim Allaoui, Nicola L Jones, Gabriel Nu&#241;ez, Stephen E Girardin &amp; Dana J Philpott</p>
<img src="http://feeds.feedburner.com/~r/ni/rss/aop/~4/0B5CognjkQQ" height="1" width="1"/>]]></content:encoded>
<dc:title>Nod1 and Nod2 direct autophagy by recruiting ATG16L1 to the plasma membrane at the site of bacterial entry</dc:title>
<dc:creator>Leonardo H Travassos</dc:creator>
<dc:creator>Leticia A M Carneiro</dc:creator>
<dc:creator>Mahendrasingh Ramjeet</dc:creator>
<dc:creator>Seamus Hussey</dc:creator>
<dc:creator>Yun-Gi Kim</dc:creator>
<dc:creator>João G Magalhães</dc:creator>
<dc:creator>Linda Yuan</dc:creator>
<dc:creator>Fraser Soares</dc:creator>
<dc:creator>Evelyn Chea</dc:creator>
<dc:creator>Lionel Le Bourhis</dc:creator>
<dc:creator>Ivo G Boneca</dc:creator>
<dc:creator>Abdelmounaaim Allaoui</dc:creator>
<dc:creator>Nicola L Jones</dc:creator>
<dc:creator>Gabriel Nuñez</dc:creator>
<dc:creator>Stephen E Girardin</dc:creator>
<dc:creator>Dana J Philpott</dc:creator>
<dc:identifier>doi:10.1038/ni.1823</dc:identifier>
<dc:source>Nature Immunology</dc:source>
<dc:date>2009-11-08</dc:date>
<prism:publicationName>Nature Immunology</prism:publicationName>
<prism:publicationDate>2009-11-08</prism:publicationDate>
<prism:doi>10.1038/ni.1823</prism:doi>
<prism:url>http://dx.doi.org/10.1038/ni.1823</prism:url>
<prism:section>Article</prism:section>
<prism:startingPage />
<prism:endingPage />
<feedburner:origLink>http://dx.doi.org/10.1038/ni.1823</feedburner:origLink></item>
<item rdf:about="http://dx.doi.org/10.1038/ni.1819">
<title>Different modes of ubiquitination of the adaptor TRAF3 selectively activate the expression of type I interferons and proinflammatory cytokines</title>
<link>http://feeds.nature.com/~r/ni/rss/aop/~3/Dfk3IwXtjEc/ni.1819</link>
<description>TLR4 signals via MyD88 and TRIF to activate proinflammatory cytokine and type I interferon responses. Karin and colleagues show that different ubiquitination of TRAF3 via K48 or K63 dictates the ensuing immune response.</description>
<content:encoded><![CDATA[
<div><a href="http://ad.doubleclick.net/adj/ni.nature.com/rss;sz=728x90"><img src="http://ad.doubleclick.net/ad/ni.nature.com/rss;sz=728x90" alt="Advertisement" style="border:0" /></a></div>
<p>
<b>Different modes of ubiquitination of the adaptor TRAF3 selectively activate the expression of type I interferons and proinflammatory cytokines</b>
</p>
<p>Nature Immunology. <a href="http://dx.doi.org/10.1038/ni.1819">doi:10.1038/ni.1819</a>
</p>
<p>Authors: Ping-Hui Tseng, Atsushi Matsuzawa, Weizhou Zhang, Takashi Mino, Dario A A Vignali &amp; Michael Karin</p>
<img src="http://feeds.feedburner.com/~r/ni/rss/aop/~4/Dfk3IwXtjEc" height="1" width="1"/>]]></content:encoded>
<dc:title>Different modes of ubiquitination of the adaptor TRAF3 selectively activate the expression of type I interferons and proinflammatory cytokines</dc:title>
<dc:creator>Ping-Hui Tseng</dc:creator>
<dc:creator>Atsushi Matsuzawa</dc:creator>
<dc:creator>Weizhou Zhang</dc:creator>
<dc:creator>Takashi Mino</dc:creator>
<dc:creator>Dario A A Vignali</dc:creator>
<dc:creator>Michael Karin</dc:creator>
<dc:identifier>doi:10.1038/ni.1819</dc:identifier>
<dc:source>Nature Immunology</dc:source>
<dc:date>2009-11-08</dc:date>
<prism:publicationName>Nature Immunology</prism:publicationName>
<prism:publicationDate>2009-11-08</prism:publicationDate>
<prism:doi>10.1038/ni.1819</prism:doi>
<prism:url>http://dx.doi.org/10.1038/ni.1819</prism:url>
<prism:section>Article</prism:section>
<prism:startingPage />
<prism:endingPage />
<feedburner:origLink>http://dx.doi.org/10.1038/ni.1819</feedburner:origLink></item>
<item rdf:about="http://dx.doi.org/10.1038/ni.1825">
<title>Enteric defensins are essential regulators of intestinal microbial ecology</title>
<link>http://feeds.nature.com/~r/ni/rss/aop/~3/PjvDIecslaM/ni.1825</link>
<description>Defensins combat pathogenic bacteria invading the mammalian intestine. Salzman and co-workers find that defensins influence the composition of the small intestinal commensal microbiota and the presence of interleukin 17–producing T cells in the lamina propria.</description>
<content:encoded><![CDATA[
<div><a href="http://ad.doubleclick.net/adj/ni.nature.com/rss;sz=728x90"><img src="http://ad.doubleclick.net/ad/ni.nature.com/rss;sz=728x90" alt="Advertisement" style="border:0" /></a></div>
<p>
<b>Enteric defensins are essential regulators of intestinal microbial ecology</b>
</p>
<p>Nature Immunology. <a href="http://dx.doi.org/10.1038/ni.1825">doi:10.1038/ni.1825</a>
</p>
<p>Authors: Nita H Salzman, Kuiechun Hung, Dipica Haribhai, Hiutung Chu, Jenny Karlsson-Sj&#246;berg, Elad Amir, Paul Teggatz, Melissa Barman, Michael Hayward, Daniel Eastwood, Maaike Stoel, Yanjiao Zhou, Erica Sodergren, George M Weinstock, Charles L Bevins, Calvin B Williams &amp; Nicolaas A Bos</p>
<img src="http://feeds.feedburner.com/~r/ni/rss/aop/~4/PjvDIecslaM" height="1" width="1"/>]]></content:encoded>
<dc:title>Enteric defensins are essential regulators of intestinal microbial ecology</dc:title>
<dc:creator>Nita H Salzman</dc:creator>
<dc:creator>Kuiechun Hung</dc:creator>
<dc:creator>Dipica Haribhai</dc:creator>
<dc:creator>Hiutung Chu</dc:creator>
<dc:creator>Jenny Karlsson-Sjöberg</dc:creator>
<dc:creator>Elad Amir</dc:creator>
<dc:creator>Paul Teggatz</dc:creator>
<dc:creator>Melissa Barman</dc:creator>
<dc:creator>Michael Hayward</dc:creator>
<dc:creator>Daniel Eastwood</dc:creator>
<dc:creator>Maaike Stoel</dc:creator>
<dc:creator>Yanjiao Zhou</dc:creator>
<dc:creator>Erica Sodergren</dc:creator>
<dc:creator>George M Weinstock</dc:creator>
<dc:creator>Charles L Bevins</dc:creator>
<dc:creator>Calvin B Williams</dc:creator>
<dc:creator>Nicolaas A Bos</dc:creator>
<dc:identifier>doi:10.1038/ni.1825</dc:identifier>
<dc:source>Nature Immunology</dc:source>
<dc:date>2009-10-22</dc:date>
<prism:publicationName>Nature Immunology</prism:publicationName>
<prism:publicationDate>2009-10-22</prism:publicationDate>
<prism:doi>10.1038/ni.1825</prism:doi>
<prism:url>http://dx.doi.org/10.1038/ni.1825</prism:url>
<prism:section>Article</prism:section>
<prism:startingPage />
<prism:endingPage />
<feedburner:origLink>http://dx.doi.org/10.1038/ni.1825</feedburner:origLink></item>
</rdf:RDF>
