Dergi makalesi Açık Erişim
Koyas, Altay; Tucer, Suat; Kayhan, Merve; Savas, Ali Can; Akdemir, Imran; Cekic, Caglar
<?xml version='1.0' encoding='utf-8'?> <oai_dc:dc xmlns:dc="http://purl.org/dc/elements/1.1/" xmlns:oai_dc="http://www.openarchives.org/OAI/2.0/oai_dc/" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance" xsi:schemaLocation="http://www.openarchives.org/OAI/2.0/oai_dc/ http://www.openarchives.org/OAI/2.0/oai_dc.xsd"> <dc:creator>Koyas, Altay</dc:creator> <dc:creator>Tucer, Suat</dc:creator> <dc:creator>Kayhan, Merve</dc:creator> <dc:creator>Savas, Ali Can</dc:creator> <dc:creator>Akdemir, Imran</dc:creator> <dc:creator>Cekic, Caglar</dc:creator> <dc:date>2021-01-01</dc:date> <dc:description>The nucleoside adenosine accumulates extracellularly in solid tumors and inhibits CD8(+) T cells by activating adenosine receptors. The cytokine interleukin-7 (IL-7), which is produced by various tissues and tumors, promotes the survival and maintenance of T cells. Adenosine and IL-7 signaling are being clinically targeted separately or in combination with other therapies for solid tumor indications. Here, we found that IL-7 signaling promoted the accumulation of tumor-associated CD8(+) T cells, in part, by preventing adenosine-mediated immunosuppression. Inhibition of the transcription factor FoxO1 downstream of IL-7 receptor signaling was important for protecting CD8(+) T cells from suppression by adenosine. These findings have implications for the development of new approaches for cancer immunotherapies that target the adenosine pathway.</dc:description> <dc:identifier>https://aperta.ulakbim.gov.trrecord/239106</dc:identifier> <dc:identifier>oai:aperta.ulakbim.gov.tr:239106</dc:identifier> <dc:rights>info:eu-repo/semantics/openAccess</dc:rights> <dc:rights>http://www.opendefinition.org/licenses/cc-by</dc:rights> <dc:source>SCIENCE SIGNALING 14(674)</dc:source> <dc:title>Interleukin-7 protects CD8(+) T cells from adenosine-mediated immunosuppression</dc:title> <dc:type>info:eu-repo/semantics/article</dc:type> <dc:type>publication-article</dc:type> </oai_dc:dc>
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