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<title>Volume 13, Issue 4 (2017) | American Journal of Immunology</title>
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    <title><![CDATA[Involvement of the α/β Isoform of p38 MAP Kinase in Chemotactic Responses of Human Eosinophils to Eotaxin (CCL11) and RANTES (CCL5)]]></title>
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        <![CDATA[<p>American Journal of Immunology, Published online: 26 October 2017; <a href="https://thescipub.com/aji/ajisp.2017.209.215">doi:10.3844/ajisp.2017.209.215</a></p>Eosinophils are the principal effector cells for allergic inflammation in a variety of diseases, in which they contribute to tissue damage and remodelling processes via the secretion of cytotoxic gran...]]></content:encoded>
    <dc:title><![CDATA[Involvement of the α/β Isoform of p38 MAP Kinase in Chemotactic Responses of Human Eosinophils to Eotaxin (CCL11) and RANTES (CCL5)]]></dc:title><dc:creator>Anwar M Hasan</dc:creator><dc:creator>Gordon  Dent</dc:creator><dc:identifier>doi:10.3844/ajisp.2017.209.215</dc:identifier>
    <dc:source>American Journal of Immunology, Published online: 2017-10-26; | doi:10.3844/ajisp.2017.209.215</dc:source>
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    <title><![CDATA[The Arid3a Transcription Factor Rescues Natural and RAS-V12-Induced Senescence Via a Rb-Dependent Pathway]]></title>
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        <![CDATA[<p>American Journal of Immunology, Published online: 4 November 2017; <a href="https://thescipub.com/aji/ajisp.2017.216.232">doi:10.3844/ajisp.2017.216.232</a></p>Primary cells are protected against oncogenic events by undergoing premature cellular senescence—an irreversible cell cycle arrest activated by mitogenic signaling as well as by overexpression of tu...]]></content:encoded>
    <dc:title><![CDATA[The Arid3a Transcription Factor Rescues Natural and RAS-V12-Induced Senescence Via a Rb-Dependent Pathway]]></dc:title><dc:creator>Christian  Schmidt</dc:creator><dc:creator>Dongkyoon  Kim</dc:creator><dc:creator>Shawn  Mathur</dc:creator><dc:creator>David  Covarrubias</dc:creator><dc:creator>Chhaya  Das</dc:creator><dc:creator>Mark A. Brown</dc:creator><dc:creator>Joachim  Storsberg</dc:creator><dc:creator>Haley O. Tucker</dc:creator><dc:identifier>doi:10.3844/ajisp.2017.216.232</dc:identifier>
    <dc:source>American Journal of Immunology, Published online: 2017-11-04; | doi:10.3844/ajisp.2017.216.232</dc:source>
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    <title><![CDATA[The Triple Immune Argument; Surveillance/Evasion/ Senescence and the Increased Incidence of Acute Myeloid Leukemia Observed with Age]]></title>
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        <![CDATA[<p>American Journal of Immunology, Published online: 22 December 2017; <a href="https://thescipub.com/aji/ajisp.2017.233.252">doi:10.3844/ajisp.2017.233.252</a></p>AML originates from genetic insults of hematopoietic stem and progenitor cells (HSPCs/HSCs) that was identified earlier as leukemia stem cells (LSCs). In quiescent state, trafficking immune cells are ...]]></content:encoded>
    <dc:title><![CDATA[The Triple Immune Argument; Surveillance/Evasion/ Senescence and the Increased Incidence of Acute Myeloid Leukemia Observed with Age]]></dc:title><dc:creator>Manar M. Ismail</dc:creator><dc:identifier>doi:10.3844/ajisp.2017.233.252</dc:identifier>
    <dc:source>American Journal of Immunology, Published online: 2017-12-22; | doi:10.3844/ajisp.2017.233.252</dc:source>
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