Bcr/Abl-induced deregulation of the IL-33/ST2 pathway in CD34(+) progenitors from chronic myeloid leukemia patients (P6284)
In: The Journal of Immunology, Jg. 190 (2013-05-01), S. 46.13
Online
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Zugriff:
Although it is generally acknowledged that cytokines regulate normal hematopoiesis in an autocrine/paracrine fashion, their possible role in chronic myeloid leukemia (CML) and resistance to imatinib mesylate (IM) treatment remain poorly investigated. Here, we report that CD34(+) progenitors from CML patients at diagnosis are selectively targeted by the cytokine/alarmin IL-33. Indeed, CML CD34(+) progenitors up-regulate their cell surface expression of the IL-33-specific receptor chain ST2, proliferate and produce cytokines in response to IL-33, conversely to CD34(+) cells from healthy individuals. Moreover, ST2 overexpression is normalized following IM therapy, while IL-33 counteracts in-vitro IM-induced growth arrest in CML CD34(+) progenitors via re-activation of the STAT5 pathway. Clinically, CML is associated with high circulating levels of soluble ST2, commonly used as a functional signature of IL-33 signaling in vivo. Taken together, our results support the hypothesis that the IL-33/ST2 pathway facilitates Bcr/Abl-induced leukemogenesis and contributes to IM resistance in CML patients.
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Bcr/Abl-induced deregulation of the IL-33/ST2 pathway in CD34(+) progenitors from chronic myeloid leukemia patients (P6284)
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Autor/in / Beteiligte Person: | Gombert, Jean-Marc ; Levescot, Anaïs ; Flamant, Stéphane ; Jacomet, Florence ; Basbous, Sara ; Féraud, Olivier ; Bonnet, Marie-Laure ; Giraud, Christine ; Roy, Lydia ; Barra, Anne ; Turhan, Ali ; Guilhot, François ; Herbelin, André |
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Zeitschrift: | The Journal of Immunology, Jg. 190 (2013-05-01), S. 46.13 |
Veröffentlichung: | The American Association of Immunologists, 2013 |
Medientyp: | unknown |
ISSN: | 1550-6606 (print) ; 0022-1767 (print) |
DOI: | 10.4049/jimmunol.190.supp.46.13 |
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