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	<title>CiteULike: AlfonsoVicenteSuarezs Trinchieri</title>
	<description>CiteULike: AlfonsoVicenteSuarezs Trinchieri</description>


	<link>http://www.citeulike.org/user/AlfonsoVicenteSuarez/author/Trinchieri</link>
	<dc:publisher>CiteULike.org</dc:publisher>
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        <rdf:li rdf:resource="http://www.citeulike.org/user/AlfonsoVicenteSuarez/article/329642"/>
        <rdf:li rdf:resource="http://www.citeulike.org/user/AlfonsoVicenteSuarez/article/1688016"/>
        <rdf:li rdf:resource="http://www.citeulike.org/user/AlfonsoVicenteSuarez/article/1402638"/>
        <rdf:li rdf:resource="http://www.citeulike.org/user/AlfonsoVicenteSuarez/article/1402623"/>
        <rdf:li rdf:resource="http://www.citeulike.org/user/AlfonsoVicenteSuarez/article/1387964"/>
        <rdf:li rdf:resource="http://www.citeulike.org/user/AlfonsoVicenteSuarez/article/1387960"/>
        <rdf:li rdf:resource="http://www.citeulike.org/user/AlfonsoVicenteSuarez/article/1387806"/>
        <rdf:li rdf:resource="http://www.citeulike.org/user/AlfonsoVicenteSuarez/article/1387797"/>
        <rdf:li rdf:resource="http://www.citeulike.org/user/AlfonsoVicenteSuarez/article/1119389"/>

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<item rdf:about="http://www.citeulike.org/user/AlfonsoVicenteSuarez/article/329642">
    <title>Interaction between conventional dendritic cells and natural killer cells is integral to the activation of effective antiviral immunity</title>
    <link>http://www.citeulike.org/user/AlfonsoVicenteSuarez/article/329642</link>
    <description>&lt;i&gt;Nature Immunology, Vol. 6, No. 10. (04 September 2005), pp. 1011-1019.&lt;/i&gt;</description>
    <dc:title>Interaction between conventional dendritic cells and natural killer cells is integral to the activation of effective antiviral immunity</dc:title>

    <dc:creator>Christopher Andoniou</dc:creator>
    <dc:creator>Serani van Dommelen</dc:creator>
    <dc:creator>Valentina Voigt</dc:creator>
    <dc:creator>Daniel Andrews</dc:creator>
    <dc:creator>Geraldine Brizard</dc:creator>
    <dc:creator>Carine Asselin-Paturel</dc:creator>
    <dc:creator>Thomas Delale</dc:creator>
    <dc:creator>Katryn Stacey</dc:creator>
    <dc:creator>Giorgio Trinchieri</dc:creator>
    <dc:creator>Mariapia Degli-Esposti</dc:creator>
    <dc:identifier>doi:10.1038/ni1244</dc:identifier>
    <dc:source>Nature Immunology, Vol. 6, No. 10. (04 September 2005), pp. 1011-1019.</dc:source>
    <dc:date>2005-09-22T05:54:07-00:00</dc:date>
    <prism:publicationName>Nature Immunology</prism:publicationName>
    <prism:issn>1529-2908</prism:issn>
    <prism:volume>6</prism:volume>
    <prism:number>10</prism:number>
    <prism:startingPage>1011</prism:startingPage>
    <prism:endingPage>1019</prism:endingPage>
    <prism:publisher>Nature Publishing Group</prism:publisher>
    <prism:category>ra</prism:category>
    <prism:category>rae-1</prism:category>
</item>



<item rdf:about="http://www.citeulike.org/user/AlfonsoVicenteSuarez/article/1688016">
    <title>Reversal of Tumor-induced Dendritic Cell Paralysis by CpG Immunostimulatory Oligonucleotide and Anti-Interleukin 10 Receptor Antibody</title>
    <link>http://www.citeulike.org/user/AlfonsoVicenteSuarez/article/1688016</link>
    <description>&lt;i&gt;J. Exp. Med., Vol. 196, No. 4. (19 August 2002), pp. 541-549.&lt;/i&gt;&lt;br /&gt;&lt;br /&gt;Progressing tumors in man and mouse are often infiltrated by dendritic cells (DCs). Deficient antitumor immunity could be related to a lack of tumor-associated antigen (TAA) presentation by tumor-infiltrating DCs (TIDCs) or to a functional defect of TIDCs. Here we investigated the phenotype and function of TIDCs in transplantable and transgenic mouse tumor models. Although TIDCs could encompass various known DC subsets, most had an immature phenotype. We observed that TIDCs were able to present TAA in the context of major histocompatibility complex class I but that they were refractory to stimulation with the combination of lipopolysaccharide, interferon gamma, and anti-CD40 antibody. We could revert TIDC paralysis, however, by in vitro or in vivo stimulation with the combination of a CpG immunostimulatory sequence and an anti-interleukin 10 receptor (IL-10R) antibody. CpG or anti-IL-10R alone were inactive in TIDCs, whereas CpG triggered activation in normal DCs. In particular, CpG plus anti-IL-10R enhanced the TAA-specific immune response and triggered de novo IL-12 production. Subsequently, CpG plus anti-IL-10R treatment showed robust antitumor therapeutic activity exceeding by far that of CpG alone, and elicited antitumor immune memory. 10.1084/jem.20020732</description>
    <dc:title>Reversal of Tumor-induced Dendritic Cell Paralysis by CpG Immunostimulatory Oligonucleotide and Anti-Interleukin 10 Receptor Antibody</dc:title>

    <dc:creator>Alain Vicari</dc:creator>
    <dc:creator>Claudia Chiodoni</dc:creator>
    <dc:creator>Celine Vaure</dc:creator>
    <dc:creator>Smina Ait-Yahia</dc:creator>
    <dc:creator>Christophe Dercamp</dc:creator>
    <dc:creator>Fabien Matsos</dc:creator>
    <dc:creator>Olivier Reynard</dc:creator>
    <dc:creator>Catherine Taverne</dc:creator>
    <dc:creator>Philippe Merle</dc:creator>
    <dc:creator>Mario Colombo</dc:creator>
    <dc:creator>Anne O'Garra</dc:creator>
    <dc:creator>Giorgio Trinchieri</dc:creator>
    <dc:creator>Christophe Caux</dc:creator>
    <dc:identifier>doi:10.1084/jem.20020732</dc:identifier>
    <dc:source>J. Exp. Med., Vol. 196, No. 4. (19 August 2002), pp. 541-549.</dc:source>
    <dc:date>2007-09-23T22:45:31-00:00</dc:date>
    <prism:publicationName>J. Exp. Med.</prism:publicationName>
    <prism:volume>196</prism:volume>
    <prism:number>4</prism:number>
    <prism:startingPage>541</prism:startingPage>
    <prism:endingPage>549</prism:endingPage>
    <prism:category>tolerogenic-dcs</prism:category>
    <prism:category>tumor-dcs</prism:category>
</item>



<item rdf:about="http://www.citeulike.org/user/AlfonsoVicenteSuarez/article/1402638">
    <title>Regulatory Role of T Cells Producing both Interferon gamma and Interleukin 10 in Persistent Infection</title>
    <link>http://www.citeulike.org/user/AlfonsoVicenteSuarez/article/1402638</link>
    <description>&lt;i&gt;J. Exp. Med., Vol. 194, No. 10. (19 November 2001), pp. 53F-57.&lt;/i&gt;&lt;br /&gt;&lt;br /&gt;10.1084/jem.194.10.f53</description>
    <dc:title>Regulatory Role of T Cells Producing both Interferon gamma and Interleukin 10 in Persistent Infection</dc:title>

    <dc:creator>Giorgio Trinchieri</dc:creator>
    <dc:identifier>doi:10.1084/jem.194.10.f53</dc:identifier>
    <dc:source>J. Exp. Med., Vol. 194, No. 10. (19 November 2001), pp. 53F-57.</dc:source>
    <dc:date>2007-06-21T15:16:18-00:00</dc:date>
    <prism:publicationName>J. Exp. Med.</prism:publicationName>
    <prism:volume>194</prism:volume>
    <prism:number>10</prism:number>
    <prism:startingPage>53F</prism:startingPage>
    <prism:endingPage>57</prism:endingPage>
    <prism:category>il-10-tcells</prism:category>
</item>



<item rdf:about="http://www.citeulike.org/user/AlfonsoVicenteSuarez/article/1402623">
    <title>Interleukin-10 production by effector T cells: Th1 cells show self control</title>
    <link>http://www.citeulike.org/user/AlfonsoVicenteSuarez/article/1402623</link>
    <description>&lt;i&gt;J. Exp. Med., Vol. 204, No. 2. (19 February 2007), pp. 239-243.&lt;/i&gt;&lt;br /&gt;&lt;br /&gt;Interleukin (IL)-10 is a cytokine that modulates both innate and adaptive immunity, primarily by exerting antiinflammatory effects. IL-10 was originally thought to be produced only by T helper (Th)2 cells, but is now known to be made by a variety of cell types. During many infections, CD4+ T cells produce both interferon (IFN)-gamma, the signature Th1 cytokine, and IL-10. New data now show that the IL-10 produced by effector Th1 cells helps limit the collateral damage caused by exaggerated inflammation. But this control may also limit the effectiveness of the immune response, resulting in a failure to fully eliminate pathogens. 10.1084/jem.20070104</description>
    <dc:title>Interleukin-10 production by effector T cells: Th1 cells show self control</dc:title>

    <dc:creator>Giorgio Trinchieri</dc:creator>
    <dc:identifier>doi:10.1084/jem.20070104</dc:identifier>
    <dc:source>J. Exp. Med., Vol. 204, No. 2. (19 February 2007), pp. 239-243.</dc:source>
    <dc:date>2007-06-21T15:06:46-00:00</dc:date>
    <prism:publicationName>J. Exp. Med.</prism:publicationName>
    <prism:volume>204</prism:volume>
    <prism:number>2</prism:number>
    <prism:startingPage>239</prism:startingPage>
    <prism:endingPage>243</prism:endingPage>
    <prism:category>il-10-tcells</prism:category>
</item>



<item rdf:about="http://www.citeulike.org/user/AlfonsoVicenteSuarez/article/1387964">
    <title>Interleukin-12 in anti-tumor immunity and immunotherapy</title>
    <link>http://www.citeulike.org/user/AlfonsoVicenteSuarez/article/1387964</link>
    <description>&lt;i&gt;Cytokine &#38; Growth Factor Reviews, Vol. 13, No. 2. (April 2002), pp. 155-168.&lt;/i&gt;&lt;br /&gt;&lt;br /&gt;Interleukin-12 (IL-12) has an essential role in the interaction between the innate and adaptive arms of immunity by regulating inflammatory responses, innate resistance to infection, and adaptive immunity. Endogenous IL-12 is required for resistance to many pathogens and to transplantable and chemically induced tumors. In experimental tumor models, recombinant IL-12 treatment has a dramatic anti-tumor effect on transplantable tumors, on chemically induced tumors, and in tumors arising spontaneously in genetically modified mice. IL-12 utilizes effector mechanisms of both innate resistance and adaptive immunity to mediate anti-tumor resistance. IFN-[gamma] and a cascade of other secondary and tertiary pro-inflammatory cytokines induced by IL-12 have a direct toxic effect on the tumor cells or may activate potent anti-angiogenic mechanisms. The stimulating activity of IL-12 on antigen-specific immunity relies mostly on its ability to determine or augment Th1 and cytotoxic T lymphocyte responses. Because of this ability, IL-12 has a potent adjuvant activity in cancer and other vaccines. The promising data obtained in the pre-clinical models of anti-tumor immunotherapy have raised much hope that IL-12 could be a powerful therapeutic agent against cancer. However, excessive clinical toxicity and modest clinical response observed in the clinical trials point to the necessity to plan protocols that minimize toxicity without affecting the anti-tumor effect of IL-12.</description>
    <dc:title>Interleukin-12 in anti-tumor immunity and immunotherapy</dc:title>

    <dc:creator>Mario Colombo</dc:creator>
    <dc:creator>Giorgio Trinchieri</dc:creator>
    <dc:source>Cytokine &#38; Growth Factor Reviews, Vol. 13, No. 2. (April 2002), pp. 155-168.</dc:source>
    <dc:date>2007-06-13T17:46:43-00:00</dc:date>
    <prism:publicationName>Cytokine &#38; Growth Factor Reviews</prism:publicationName>
    <prism:volume>13</prism:volume>
    <prism:number>2</prism:number>
    <prism:startingPage>155</prism:startingPage>
    <prism:endingPage>168</prism:endingPage>
    <prism:category>il-12-general</prism:category>
</item>



<item rdf:about="http://www.citeulike.org/user/AlfonsoVicenteSuarez/article/1387960">
    <title>Tumour escape from immune surveillance through dendritic cell inactivation.</title>
    <link>http://www.citeulike.org/user/AlfonsoVicenteSuarez/article/1387960</link>
    <description>&lt;i&gt;Semin Cancer Biol, Vol. 12, No. 1. (February 2002), pp. 33-42.&lt;/i&gt;&lt;br /&gt;&lt;br /&gt;Dendritic cells (DC) are central to the initiation of immunity. To induce immune reactivity, DC are recruited at the site of antigen expression, uptake antigens and migrate to secondary lymphoid organs while receiving activation signals delivered by pathogens, dying cells, and/or T cells. Tumours can escape the immune system by interfering with the migration of DC or by not providing the necessary activation signals. Moreover, tumours promote the secretion of factors that inhibit DC differentiation and functions. We will review the current knowledge of the physiopathology of DC in cancer, which paves the way for novel strategies of therapeutic intervention.</description>
    <dc:title>Tumour escape from immune surveillance through dendritic cell inactivation.</dc:title>

    <dc:creator>AP Vicari</dc:creator>
    <dc:creator>C Caux</dc:creator>
    <dc:creator>G Trinchieri</dc:creator>
    <dc:identifier>doi:10.1006/scbi.2001.0400</dc:identifier>
    <dc:source>Semin Cancer Biol, Vol. 12, No. 1. (February 2002), pp. 33-42.</dc:source>
    <dc:date>2007-06-13T17:45:14-00:00</dc:date>
    <prism:publicationName>Semin Cancer Biol</prism:publicationName>
    <prism:issn>1044-579X</prism:issn>
    <prism:volume>12</prism:volume>
    <prism:number>1</prism:number>
    <prism:startingPage>33</prism:startingPage>
    <prism:endingPage>42</prism:endingPage>
    <prism:category>tolerogenic-dcs</prism:category>
</item>



<item rdf:about="http://www.citeulike.org/user/AlfonsoVicenteSuarez/article/1387806">
    <title>INTERLEUKIN-12 AND THE REGULATION OF INNATE RESISTANCE AND ADAPTIVE IMMUNITY</title>
    <link>http://www.citeulike.org/user/AlfonsoVicenteSuarez/article/1387806</link>
    <description>&lt;i&gt;Nat Rev Immunol, Vol. 3, No. 2. (February 2003), pp. 133-146.&lt;/i&gt;</description>
    <dc:title>INTERLEUKIN-12 AND THE REGULATION OF INNATE RESISTANCE AND ADAPTIVE IMMUNITY</dc:title>

    <dc:creator>Giorgio Trinchieri</dc:creator>
    <dc:identifier>doi:10.1038/nri1001 </dc:identifier>
    <dc:source>Nat Rev Immunol, Vol. 3, No. 2. (February 2003), pp. 133-146.</dc:source>
    <dc:date>2007-06-13T16:49:15-00:00</dc:date>
    <prism:publicationName>Nat Rev Immunol</prism:publicationName>
    <prism:volume>3</prism:volume>
    <prism:number>2</prism:number>
    <prism:startingPage>133</prism:startingPage>
    <prism:endingPage>146</prism:endingPage>
    <prism:category>il-12-general</prism:category>
</item>



<item rdf:about="http://www.citeulike.org/user/AlfonsoVicenteSuarez/article/1387797">
    <title>The IL-12 Family of Heterodimeric Cytokines: New Players in the Regulation of T Cell Responses</title>
    <link>http://www.citeulike.org/user/AlfonsoVicenteSuarez/article/1387797</link>
    <description>&lt;i&gt;Immunity, Vol. 19, No. 5. (November 2003), pp. 641-644.&lt;/i&gt;&lt;br /&gt;&lt;br /&gt;Originally the only known heterodimeric cytokine, IL-12 is now part of a family of five cytokines and shares important functions in the regulation of both innate and adaptive immunity with two of them, IL-23 and IL-27. Although initially these three cytokines were considered to have largely overlapping immunological functions, more recent studies, including two articles in this issue of Immunity ( and ), indicate that they mediate complex and well-differentiated functions.</description>
    <dc:title>The IL-12 Family of Heterodimeric Cytokines: New Players in the Regulation of T Cell Responses</dc:title>

    <dc:creator>Giorgio Trinchieri</dc:creator>
    <dc:creator>Stefan Pflanz</dc:creator>
    <dc:creator>Robert Kastelein</dc:creator>
    <dc:source>Immunity, Vol. 19, No. 5. (November 2003), pp. 641-644.</dc:source>
    <dc:date>2007-06-13T16:42:37-00:00</dc:date>
    <prism:publicationName>Immunity</prism:publicationName>
    <prism:volume>19</prism:volume>
    <prism:number>5</prism:number>
    <prism:startingPage>641</prism:startingPage>
    <prism:endingPage>644</prism:endingPage>
    <prism:category>il-12-general</prism:category>
</item>



<item rdf:about="http://www.citeulike.org/user/AlfonsoVicenteSuarez/article/1119389">
    <title>Cooperation of Toll-like receptor signals in innate immune defence</title>
    <link>http://www.citeulike.org/user/AlfonsoVicenteSuarez/article/1119389</link>
    <description>&lt;i&gt;Nature Reviews Immunology, Vol. 7, No. 3., pp. 179-190.&lt;/i&gt;</description>
    <dc:title>Cooperation of Toll-like receptor signals in innate immune defence</dc:title>

    <dc:creator>Giorgio Trinchieri</dc:creator>
    <dc:creator>Alan Sher</dc:creator>
    <dc:identifier>doi:10.1038/nri2038</dc:identifier>
    <dc:source>Nature Reviews Immunology, Vol. 7, No. 3., pp. 179-190.</dc:source>
    <dc:date>2007-02-23T22:17:07-00:00</dc:date>
    <prism:publicationName>Nature Reviews Immunology</prism:publicationName>
    <prism:issn>1474-1733</prism:issn>
    <prism:volume>7</prism:volume>
    <prism:number>3</prism:number>
    <prism:startingPage>179</prism:startingPage>
    <prism:endingPage>190</prism:endingPage>
    <prism:publisher>Nature Publishing Group</prism:publisher>
    <prism:category>tlr-signaling</prism:category>
</item>



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