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Gabrusiewicz, Konrad; Li, Xu; Wei, Jun; Hashimoto, Yuuri; Marisetty, Anantha L.; Ott, Martina; Wang, Fei; Hawke, David; Yu, John; Healy, Luke M.; Hossain, Anwar; Akers, Johnny C.; Maiti, Sourindra N.; Yamashita, Shinji; Shimizu, Yuzaburo; Dunner, Kenneth; Zal, M. Anna; Burks, Jared K.; Gumin, Joy; Nwajei, Felix; Rezavanian, Aras; Zhou, Shouhao; Rao, Ganesh; Sawaya, Raymond; Fuller, Gregory N.; Huse, Jason T.; Antel, Jack P.; Li, Shulin; Cooper, Laurence; Sulman, Erik P.; Chen, Clark; Geula, Changiz; Kalluri, Raghu; Zal, Tomasz; Heimberger, Amy B.
Oncoimmunology, 04/2018, Letnik: 7, Številka: 4Journal Article
Exosomes can mediate a dynamic method of communication between malignancies, including those sequestered in the central nervous system and the immune system. We sought to determine whether exosomes from glioblastoma (GBM)-derived stem cells (GSCs) can induce immunosuppression. We report that GSC-derived exosomes (GDEs) have a predilection for monocytes, the precursor to macrophages. The GDEs traverse the monocyte cytoplasm, cause a reorganization of the actin cytoskeleton, and skew monocytes toward the immune suppresive M2 phenotype, including programmed death-ligand 1 (PD-L1) expression. Mass spectrometry analysis demonstrated that the GDEs contain a variety of components, including members of the signal transducer and activator of transcription 3 (STAT3) pathway that functionally mediate this immune suppressive switch. Western blot analysis revealed that upregulation of PD-L1 in GSC exosome-treated monocytes and GBM-patient-infiltrating CD14 + cells predominantly correlates with increased phosphorylation of STAT3, and in some cases, with phosphorylated p70S6 kinase and Erk1/2. Cumulatively, these data indicate that GDEs are secreted GBM-released factors that are potent modulators of the GBM-associated immunosuppressive microenvironment.
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JCR | SNIP | JCR | SNIP | JCR | SNIP | JCR | SNIP |
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Vir: Osebne bibliografije
in: SICRIS
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