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<b>Resolving inflammation: dual anti-inflammatory and pro-resolution lipid mediators</b>
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<p>Nature Reviews Immunology 8, 349 (2008). <a href="http://dx.doi.org/10.1038/nri2294">doi:10.1038/nri2294</a>
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<b>TH17 cells in development: an updated view of their molecular identity and genetic programming</b>
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<p>Nature Reviews Immunology 8, 337 (2008). <a href="http://dx.doi.org/10.1038/nri2295">doi:10.1038/nri2295</a>
</p>
<p>Author: Chen Dong</p>
<p>Following activation, CD4+ T cells differentiate into different lineages of helper T (TH) cells that are characterized by distinct developmental regulation and biological functions. TH17 cells have recently been identified as a new lineage of effector TH</p>
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<dc:title>TH17 cells in development: an updated view of their molecular identity and genetic programming</dc:title>
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<description>Inflammation is a crucial element of the host response to cellular insult. Pathogen-induced inflammation includes a molecular pathway which proceeds through activation of the protease caspase-1 to the release of the inflammatory cytokines interleukin-1 (IL-1) and IL-18. Importantly, pathogens may also induce forms of cell </description>
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<b>NLRs at the intersection of cell death and immunity</b>
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<p>Nature Reviews Immunology 8, 372 (2008). <a href="http://dx.doi.org/10.1038/nri2296">doi:10.1038/nri2296</a>
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<p>Authors: Jenny P.-Y. Ting, Stephen B. Willingham
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<p>Inflammation is a crucial element of the host response to cellular insult. Pathogen-induced inflammation includes a molecular pathway which proceeds through activation of the protease caspase-1 to the release of the inflammatory cytokines interleukin-1 (IL-1) and IL-18. Importantly, pathogens may also induce forms of cell </p>
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<description>A key feature of the immune system is its ability to induce protective immunity against pathogens while maintaining tolerance towards self and innocuous environmental antigens. Recent evidence suggests that by guiding cells to and within lymphoid organs, CC-chemokine receptor 7 (CCR7) essentially contributes to both </description>
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<b>CCR7 and its ligands: balancing immunity and tolerance</b>
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<p>Nature Reviews Immunology 8, 362 (2008). <a href="http://dx.doi.org/10.1038/nri2297">doi:10.1038/nri2297</a>
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<p>A key feature of the immune system is its ability to induce protective immunity against pathogens while maintaining tolerance towards self and innocuous environmental antigens. Recent evidence suggests that by guiding cells to and within lymphoid organs, CC-chemokine receptor 7 (CCR7) essentially contributes to both </p>
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<description>Recent studies have revealed that the TAM receptor protein tyrosine kinases &#8212; TYRO3, AXL and MER &#8212; have pivotal roles in innate immunity. They inhibit inflammation in dendritic cells and macrophages, promote the phagocytosis of apoptotic cells and membranous organelles, and stimulate the maturation of </description>
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<b>Immunobiology of the TAM receptors</b>
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<p>Nature Reviews Immunology 8, 327 (2008). <a href="http://dx.doi.org/10.1038/nri2303">doi:10.1038/nri2303</a>
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<description>T-cell acute lymphoblastic leukaemia (T-ALL) is induced by the transformation of T-cell progenitors and mainly occurs in children and adolescents. Although treatment outcome in patients with T-ALL has improved in recent years, patients with relapsed disease continue to have a poor prognosis. It is therefore </description>
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<p>
<b>Molecular pathogenesis of T-cell leukaemia and lymphoma</b>
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<p>Nature Reviews Immunology 8, 380 (2008). <a href="http://dx.doi.org/10.1038/nri2304">doi:10.1038/nri2304</a>
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<p>T-cell acute lymphoblastic leukaemia (T-ALL) is induced by the transformation of T-cell progenitors and mainly occurs in children and adolescents. Although treatment outcome in patients with T-ALL has improved in recent years, patients with relapsed disease continue to have a poor prognosis. It is therefore </p>
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<dc:title>Molecular pathogenesis of T-cell leukaemia and lymphoma</dc:title>
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<description>When B cells react aggressively against self, the potential for pathology is extreme. It is therefore not surprising that B-cell depletion is seen as an attractive therapy in autoimmune diseases. However, B cells can also be essential for restraining unwanted autoaggressive T-cell responses. Recent advances </description>
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<p>
<b>Not always the bad guys: B cells as regulators of autoimmune pathology</b>
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<p>Nature Reviews Immunology 8, 391 (2008). <a href="http://dx.doi.org/10.1038/nri2315">doi:10.1038/nri2315</a>
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<p>When B cells react aggressively against self, the potential for pathology is extreme. It is therefore not surprising that B-cell depletion is seen as an attractive therapy in autoimmune diseases. However, B cells can also be essential for restraining unwanted autoaggressive T-cell responses. Recent advances </p>
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<dc:title>Not always the bad guys: B cells as regulators of autoimmune pathology</dc:title>
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<title>Vaccines: Explaining alum: immunologists' dirty little secret</title>
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<description>Aluminum hydroxide (alum) is a widely used adjuvant in human vaccines, but its mechanism of action remains ill-defined. In a new study, Lambrecht and colleagues find that a key factor in the adjuvant activity of alum is the activation of a population of inflammatory dendritic </description>
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<p>
<b>Vaccines: Explaining alum: immunologists' dirty little secret</b>
</p>
<p>Nature Reviews Immunology 8, 320 (2008). <a href="http://dx.doi.org/10.1038/nri2317">doi:10.1038/nri2317</a>
</p>
<p>Author: Sarah Allan</p>
<p>Aluminum hydroxide (alum) is a widely used adjuvant in human vaccines, but its mechanism of action remains ill-defined. In a new study, Lambrecht and colleagues find that a key factor in the adjuvant activity of alum is the activation of a population of inflammatory dendritic </p>
]]></content:encoded>
<dc:title>Vaccines: Explaining alum: immunologists' dirty little secret</dc:title>
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<description>Based on their respective roles in immune tolerance and inflammation, regulatory T (TReg) cells and interleukin-17 (IL-17)-producing CD4+ T helper cells (TH17 cells) are areas of intensive study. Two new reports in Nature have now identified the aryl </description>
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<p>
<b>T cells: Tuning T cells through the aryl hydrocarbon receptor</b>
</p>
<p>Nature Reviews Immunology 8, 326 (2008). <a href="http://dx.doi.org/10.1038/nri2319">doi:10.1038/nri2319</a>
</p>
<p>Author: Sarah Allan</p>
<p>Based on their respective roles in immune tolerance and inflammation, regulatory T (TReg) cells and interleukin-17 (IL-17)-producing CD4+ T helper cells (TH17 cells) are areas of intensive study. Two new reports in Nature have now identified the aryl </p>
]]></content:encoded>
<dc:title>T cells: Tuning T cells through the aryl hydrocarbon receptor</dc:title>
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<dc:identifier>doi:10.1038/nri2319</dc:identifier>
<dc:source>Nature Reviews Immunology 8, 326 (2008)</dc:source>
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<title>T-cell activation: The waves behind the TGN1412 storm</title>
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<description>It took less than an hour to realize something had gone terribly wrong. In March 2006, six healthy volunteers of a Phase I clinical trial who had received a single infusion of the CD28 superagonistic antibody TGN1412 suffered unpredicted devastating effects that left them fighting </description>
<content:encoded><![CDATA[

<p>
<b>T-cell activation: The waves behind the TGN1412 storm</b>
</p>
<p>Nature Reviews Immunology 8, 322 (2008). <a href="http://dx.doi.org/10.1038/nri2320">doi:10.1038/nri2320</a>
</p>
<p>Author: Marta Tufet</p>
<p>It took less than an hour to realize something had gone terribly wrong. In March 2006, six healthy volunteers of a Phase I clinical trial who had received a single infusion of the CD28 superagonistic antibody TGN1412 suffered unpredicted devastating effects that left them fighting </p>
]]></content:encoded>
<dc:title>T-cell activation: The waves behind the TGN1412 storm</dc:title>
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<dc:identifier>doi:10.1038/nri2320</dc:identifier>
<dc:source>Nature Reviews Immunology 8, 322 (2008)</dc:source>
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<title>In Brief: T-cell development</title>
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<description>Nature Reviews Immunology8, 167 (2008)The transcription factor discussed in this In Brief article was incorrectly spelt throughout the article. The correct spelling is Th-POK.</description>
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<p>
<b>In Brief: T-cell development</b>
</p>
<p>Nature Reviews Immunology 8, 325 (2008). <a href="http://dx.doi.org/10.1038/nri2321">doi:10.1038/nri2321</a>
</p>
<p>Nature Reviews Immunology8, 167 (2008)The transcription factor discussed in this In Brief article was incorrectly spelt throughout the article. The correct spelling is Th-POK.</p>
]]></content:encoded>
<dc:title>In Brief: T-cell development</dc:title>
<dc:identifier>doi:10.1038/nri2321</dc:identifier>
<dc:source>Nature Reviews Immunology 8, 325 (2008)</dc:source>
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<title>Antigen presentation: Prime time: insights into cross-presentation</title>
<link>http://dx.doi.org/10.1038/nri2323</link>
<description>Cross-presentation &#8212; the display of peptides derived from exogenous antigens on MHC class I molecules &#8212; is important for effective immune responses to tumours and viral infections. Although classical antigen processing pathways are well characterized, the pathways that lead to cross-presentation are less clear. How </description>
<content:encoded><![CDATA[

<p>
<b>Antigen presentation: Prime time: insights into cross-presentation</b>
</p>
<p>Nature Reviews Immunology 8, 322 (2008). <a href="http://dx.doi.org/10.1038/nri2323">doi:10.1038/nri2323</a>
</p>
<p>Author: Sarah Allan</p>
<p>Cross-presentation &#8212; the display of peptides derived from exogenous antigens on MHC class I molecules &#8212; is important for effective immune responses to tumours and viral infections. Although classical antigen processing pathways are well characterized, the pathways that lead to cross-presentation are less clear. How </p>
]]></content:encoded>
<dc:title>Antigen presentation: Prime time: insights into cross-presentation</dc:title>
<dc:creator>Sarah Allan</dc:creator>
<dc:identifier>doi:10.1038/nri2323</dc:identifier>
<dc:source>Nature Reviews Immunology 8, 322 (2008)</dc:source>
<prism:publicationName>Nature Reviews Immunology</prism:publicationName>
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<title>Inflammation: Stopping before the damage is done</title>
<link>http://dx.doi.org/10.1038/nri2324</link>
<description>The activation of nuclear factor-&#954;B (NF-&#954;B) in response to cytokine signalling is a powerful mechanism for initiating an inflammatory immune response, but as is often the case in the immune system, with great power comes the potential to cause great damage. Li and colleagues now </description>
<content:encoded><![CDATA[

<p>
<b>Inflammation: Stopping before the damage is done</b>
</p>
<p>Nature Reviews Immunology 8, 324 (2008). <a href="http://dx.doi.org/10.1038/nri2324">doi:10.1038/nri2324</a>
</p>
<p>Author: Kirsty Minton</p>
<p>The activation of nuclear factor-&#954;B (NF-&#954;B) in response to cytokine signalling is a powerful mechanism for initiating an inflammatory immune response, but as is often the case in the immune system, with great power comes the potential to cause great damage. Li and colleagues now </p>
]]></content:encoded>
<dc:title>Inflammation: Stopping before the damage is done</dc:title>
<dc:creator>Kirsty Minton</dc:creator>
<dc:identifier>doi:10.1038/nri2324</dc:identifier>
<dc:source>Nature Reviews Immunology 8, 324 (2008)</dc:source>
<prism:publicationName>Nature Reviews Immunology</prism:publicationName>
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<title>NKT cells: NKT cells join the IL-17 gang</title>
<link>http://dx.doi.org/10.1038/nri2325</link>
<description>Natural killer T (NKT) cells are a unique T-cell subset defined by the co-expression of NK-cell markers and a T-cell receptor (TCR), and are characterized by their ability to rapidly produce immunomodulatory cytokines following TCR ligation. Now, Caspi and colleagues report that one of these </description>
<content:encoded><![CDATA[

<p>
<b>NKT cells: NKT cells join the IL-17 gang</b>
</p>
<p>Nature Reviews Immunology 8, 324 (2008). <a href="http://dx.doi.org/10.1038/nri2325">doi:10.1038/nri2325</a>
</p>
<p>Author: Lucy Bird</p>
<p>Natural killer T (NKT) cells are a unique T-cell subset defined by the co-expression of NK-cell markers and a T-cell receptor (TCR), and are characterized by their ability to rapidly produce immunomodulatory cytokines following TCR ligation. Now, Caspi and colleagues report that one of these </p>
]]></content:encoded>
<dc:title>NKT cells: NKT cells join the IL-17 gang</dc:title>
<dc:creator>Lucy Bird</dc:creator>
<dc:identifier>doi:10.1038/nri2325</dc:identifier>
<dc:source>Nature Reviews Immunology 8, 324 (2008)</dc:source>
<prism:publicationName>Nature Reviews Immunology</prism:publicationName>
<prism:volume>8</prism:volume>
<prism:number>5</prism:number>
<prism:section>Research Highlight</prism:section>
<prism:startingPage>324</prism:startingPage>
<prism:endingPage>324</prism:endingPage>
</item>
<item rdf:about="http://dx.doi.org/10.1038/nri2328">
<title>Tumour immunology: Tumour surveillance by NKG2D</title>
<link>http://dx.doi.org/10.1038/nri2328</link>
<description>Natural killer (NK) cells, as well as various T-cell subsets, express the stimulatory receptor natural-killer group 2, member D (NKG2D), which recognizes several ligands that are frequently upregulated by tumour cells. The expression of NKG2D ligands by tumour cell lines has been shown to render </description>
<content:encoded><![CDATA[

<p>
<b>Tumour immunology: Tumour surveillance by NKG2D</b>
</p>
<p>Nature Reviews Immunology 8, 324 (2008). <a href="http://dx.doi.org/10.1038/nri2328">doi:10.1038/nri2328</a>
</p>
<p>Author: Olive Leavy</p>
<p>Natural killer (NK) cells, as well as various T-cell subsets, express the stimulatory receptor natural-killer group 2, member D (NKG2D), which recognizes several ligands that are frequently upregulated by tumour cells. The expression of NKG2D ligands by tumour cell lines has been shown to render </p>
]]></content:encoded>
<dc:title>Tumour immunology: Tumour surveillance by NKG2D</dc:title>
<dc:creator>Olive Leavy</dc:creator>
<dc:identifier>doi:10.1038/nri2328</dc:identifier>
<dc:source>Nature Reviews Immunology 8, 324 (2008)</dc:source>
<prism:publicationName>Nature Reviews Immunology</prism:publicationName>
<prism:volume>8</prism:volume>
<prism:number>5</prism:number>
<prism:section>Research Highlight</prism:section>
<prism:startingPage>324</prism:startingPage>
<prism:endingPage>325</prism:endingPage>
</item>
<item rdf:about="http://dx.doi.org/10.1038/nri2329">
<title>Mast cells: Food allergy unplugged</title>
<link>http://dx.doi.org/10.1038/nri2329</link>
<description>The prevalence of food allergy is on the increase. Yet how susceptible individuals become sensitized to food antigens remains poorly understood. Now, a report in The Journal of Experimental Medicine shows an important role for interleukin-9 (IL-9) and mast-cell-mediated gut leakiness in </description>
<content:encoded><![CDATA[

<p>
<b>Mast cells: Food allergy unplugged</b>
</p>
<p>Nature Reviews Immunology 8, 321 (2008). <a href="http://dx.doi.org/10.1038/nri2329">doi:10.1038/nri2329</a>
</p>
<p>Author: Lucy Bird</p>
<p>The prevalence of food allergy is on the increase. Yet how susceptible individuals become sensitized to food antigens remains poorly understood. Now, a report in The Journal of Experimental Medicine shows an important role for interleukin-9 (IL-9) and mast-cell-mediated gut leakiness in </p>
]]></content:encoded>
<dc:title>Mast cells: Food allergy unplugged</dc:title>
<dc:creator>Lucy Bird</dc:creator>
<dc:identifier>doi:10.1038/nri2329</dc:identifier>
<dc:source>Nature Reviews Immunology 8, 321 (2008)</dc:source>
<prism:publicationName>Nature Reviews Immunology</prism:publicationName>
<prism:volume>8</prism:volume>
<prism:number>5</prism:number>
<prism:section>Research Highlight</prism:section>
<prism:startingPage>321</prism:startingPage>
<prism:endingPage>321</prism:endingPage>
</item>
<item rdf:about="http://dx.doi.org/10.1038/nri2330">
<title>Immunotherapy: A mismatch that works</title>
<link>http://dx.doi.org/10.1038/nri2330</link>
<description>Mismatched MHC alleles between donor and recipient represent a major barrier for adoptive T-cell therapy for immunodeficient patients and, in the case of haematopoietic stem-cell transplantation (HSCT), can cause graft rejection and graft-versus-host disease (GVHD). Now, Zakrzewski et al. show that allogeneic, MHC-mismatched T-cell </description>
<content:encoded><![CDATA[

<p>
<b>Immunotherapy: A mismatch that works</b>
</p>
<p>Nature Reviews Immunology 8, 321 (2008). <a href="http://dx.doi.org/10.1038/nri2330">doi:10.1038/nri2330</a>
</p>
<p>Author: Olive Leavy</p>
<p>Mismatched MHC alleles between donor and recipient represent a major barrier for adoptive T-cell therapy for immunodeficient patients and, in the case of haematopoietic stem-cell transplantation (HSCT), can cause graft rejection and graft-versus-host disease (GVHD). Now, Zakrzewski et al. show that allogeneic, MHC-mismatched T-cell </p>
]]></content:encoded>
<dc:title>Immunotherapy: A mismatch that works</dc:title>
<dc:creator>Olive Leavy</dc:creator>
<dc:identifier>doi:10.1038/nri2330</dc:identifier>
<dc:source>Nature Reviews Immunology 8, 321 (2008)</dc:source>
<prism:publicationName>Nature Reviews Immunology</prism:publicationName>
<prism:volume>8</prism:volume>
<prism:number>5</prism:number>
<prism:section>Research Highlight</prism:section>
<prism:startingPage>321</prism:startingPage>
<prism:endingPage>321</prism:endingPage>
</item>
<item rdf:about="http://dx.doi.org/10.1038/nri2331">
<title>In Brief</title>
<link>http://dx.doi.org/10.1038/nri2331</link>
<description>HaematopoiesisAdult T-cell progenitors retain myeloid potential.Wada, H.et al. Nature452, 768&#8211;772 (2008)The earliest thymic progenitors for T cells possess myeloid lineage potential.Bell, J. J. &amp; Bhandoola, A.Nature452</description>
<content:encoded><![CDATA[

<p>
<b>In Brief</b>
</p>
<p>Nature Reviews Immunology 8, 325 (2008). <a href="http://dx.doi.org/10.1038/nri2331">doi:10.1038/nri2331</a>
</p>
<p>HaematopoiesisAdult T-cell progenitors retain myeloid potential.Wada, H.et al. Nature452, 768&#8211;772 (2008)The earliest thymic progenitors for T cells possess myeloid lineage potential.Bell, J. J. &amp; Bhandoola, A.Nature452</p>
]]></content:encoded>
<dc:title>In Brief</dc:title>
<dc:identifier>doi:10.1038/nri2331</dc:identifier>
<dc:source>Nature Reviews Immunology 8, 325 (2008)</dc:source>
<prism:publicationName>Nature Reviews Immunology</prism:publicationName>
<prism:volume>8</prism:volume>
<prism:number>5</prism:number>
<prism:section>Research Highlight</prism:section>
<prism:startingPage>325</prism:startingPage>
<prism:endingPage>325</prism:endingPage>
</item>
<item rdf:about="http://dx.doi.org/10.1038/nri2332">
<title>From the editors</title>
<link>http://dx.doi.org/10.1038/nri2332</link>
<description>Several articles this month relate to the theme of how our immune system is able to walk the fine line between fighting off infections and preventing bystander damage or autoimmune disease. In terms of promoting an effective immune response to infection, the newest player in </description>
<content:encoded><![CDATA[

<p>
<b>From the editors</b>
</p>
<p>Nature Reviews Immunology 8, 319 (2008). <a href="http://dx.doi.org/10.1038/nri2332">doi:10.1038/nri2332</a>
</p>
<p>Several articles this month relate to the theme of how our immune system is able to walk the fine line between fighting off infections and preventing bystander damage or autoimmune disease. In terms of promoting an effective immune response to infection, the newest player in </p>
]]></content:encoded>
<dc:title>From the editors</dc:title>
<dc:identifier>doi:10.1038/nri2332</dc:identifier>
<dc:source>Nature Reviews Immunology 8, 319 (2008)</dc:source>
<prism:publicationName>Nature Reviews Immunology</prism:publicationName>
<prism:volume>8</prism:volume>
<prism:number>5</prism:number>
<prism:section>From The Editors</prism:section>
<prism:startingPage>319</prism:startingPage>
<prism:endingPage>319</prism:endingPage>
</item>
<item rdf:about="http://dx.doi.org/10.1038/nri2333">
<title>Antibiotics from alligators!</title>
<link>http://dx.doi.org/10.1038/nri2333</link>
<description>The late Steve Irwin ('The Crocodile Hunter') would no doubt have been delighted to learn about recent research, presented at the American Chemical Society meeting (6&#8211;10 April) in New Orleans, USA, showing that proteins from alligator blood could pave the way for new antibiotics.Lancia </description>
<content:encoded><![CDATA[

<p>
<b>Antibiotics from alligators!</b>
</p>
<p>Nature Reviews Immunology 8, 326 (2008). <a href="http://dx.doi.org/10.1038/nri2333">doi:10.1038/nri2333</a>
</p>
<p>Author: Lucy Bird</p>
<p>The late Steve Irwin ('The Crocodile Hunter') would no doubt have been delighted to learn about recent research, presented at the American Chemical Society meeting (6&#8211;10 April) in New Orleans, USA, showing that proteins from alligator blood could pave the way for new antibiotics.Lancia </p>
]]></content:encoded>
<dc:title>Antibiotics from alligators!</dc:title>
<dc:creator>Lucy Bird</dc:creator>
<dc:identifier>doi:10.1038/nri2333</dc:identifier>
<dc:source>Nature Reviews Immunology 8, 326 (2008)</dc:source>
<prism:publicationName>Nature Reviews Immunology</prism:publicationName>
<prism:volume>8</prism:volume>
<prism:number>5</prism:number>
<prism:section>Research Highlight</prism:section>
<prism:startingPage>326</prism:startingPage>
<prism:endingPage>326</prism:endingPage>
</item>
<item rdf:about="http://dx.doi.org/10.1038/nri2334">
<title>In Brief</title>
<link>http://dx.doi.org/10.1038/nri2334</link>
<description>MHC moleculesMHC class II-peptide complexes internalize using a clathrin- and dynamin-independent endocytosis pathway.Walseng, E.et al. J. Biol. Chem.7 April 2008 (doi:10.1074/jbc.m801070200)Recycling of peptide&#8211;MHC class II complexes from the cell surface is thought to increase the </description>
<content:encoded><![CDATA[

<p>
<b>In Brief</b>
</p>
<p>Nature Reviews Immunology 8, 323 (2008). <a href="http://dx.doi.org/10.1038/nri2334">doi:10.1038/nri2334</a>
</p>
<p>MHC moleculesMHC class II-peptide complexes internalize using a clathrin- and dynamin-independent endocytosis pathway.Walseng, E.et al. J. Biol. Chem.7 April 2008 (doi:10.1074/jbc.m801070200)Recycling of peptide&#8211;MHC class II complexes from the cell surface is thought to increase the </p>
]]></content:encoded>
<dc:title>In Brief</dc:title>
<dc:identifier>doi:10.1038/nri2334</dc:identifier>
<dc:source>Nature Reviews Immunology 8, 323 (2008)</dc:source>
<prism:publicationName>Nature Reviews Immunology</prism:publicationName>
<prism:volume>8</prism:volume>
<prism:number>5</prism:number>
<prism:section>Research Highlight</prism:section>
<prism:startingPage>323</prism:startingPage>
<prism:endingPage>323</prism:endingPage>
</item>
</rdf:RDF>
