Myeloid loss of Beclin 1 promotes PD-L1hi precursor B cell lymphoma development
Identifieur interne : 004007 ( Main/Curation ); précédent : 004006; suivant : 004008Myeloid loss of Beclin 1 promotes PD-L1hi precursor B cell lymphoma development
Auteurs : Peng Tan [États-Unis] ; Lian He [États-Unis] ; Changsheng Xing [États-Unis] ; Jingrong Mao [États-Unis, République populaire de Chine] ; Xiao Yu [États-Unis] ; Motao Zhu [États-Unis] ; Lixia Diao [États-Unis] ; Leng Han [États-Unis] ; Yubin Zhou [États-Unis] ; M. James You [États-Unis] ; Helen Y. Wang [États-Unis] ; Rong-Fu Wang [États-Unis]Source :
- The Journal of Clinical Investigation [ 0021-9738 ] ; ????.
Abstract
Beclin 1 (Becn1) is a key molecule in the autophagy pathway and has been implicated in cancer development. Due to the embryonic lethality of homozygous Becn1-deficient mice, the precise mechanisms and cell type–specific roles of Becn1 in regulating inflammation and cancer immunity remain elusive. Here, we report that myeloid-deficient
Url:
DOI: 10.1172/JCI127721
PubMed: 31503548
PubMed Central: 6877338
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PMC:6877338Le document en format XML
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promotes PD-L1<sup>hi</sup>
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<sourceDesc><biblStruct><analytic><title xml:lang="en" level="a" type="main">Myeloid loss of <italic>Beclin 1</italic>
promotes PD-L1<sup>hi</sup>
precursor B cell lymphoma development</title>
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<author><name sortKey="Yu, Xiao" sort="Yu, Xiao" uniqKey="Yu X" first="Xiao" last="Yu">Xiao Yu</name>
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<author><name sortKey="Zhu, Motao" sort="Zhu, Motao" uniqKey="Zhu M" first="Motao" last="Zhu">Motao Zhu</name>
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<author><name sortKey="Diao, Lixia" sort="Diao, Lixia" uniqKey="Diao L" first="Lixia" last="Diao">Lixia Diao</name>
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<wicri:regionArea>Department of Bioinformatics and Computational Biology, The University of Texas MD Anderson Cancer Center, Houston, Texas</wicri:regionArea>
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<author><name sortKey="Han, Leng" sort="Han, Leng" uniqKey="Han L" first="Leng" last="Han">Leng Han</name>
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<wicri:regionArea>Department of Biochemistry and Molecular Biology, The University of Texas Health Science Center at Houston McGovern Medical School, Houston, Texas</wicri:regionArea>
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<author><name sortKey="Wang, Helen Y" sort="Wang, Helen Y" uniqKey="Wang H" first="Helen Y." last="Wang">Helen Y. Wang</name>
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<author><name sortKey="Wang, Rong Fu" sort="Wang, Rong Fu" uniqKey="Wang R" first="Rong-Fu" last="Wang">Rong-Fu Wang</name>
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<series><title level="j">The Journal of Clinical Investigation</title>
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<front><div type="abstract" xml:lang="en"><p>Beclin 1 (Becn1) is a key molecule in the autophagy pathway and has been implicated in cancer development. Due to the embryonic lethality of homozygous Becn1-deficient mice, the precise mechanisms and cell type–specific roles of Becn1 in regulating inflammation and cancer immunity remain elusive. Here, we report that myeloid-deficient <italic>Becn1</italic>
(<italic>Becn1<sup>ΔM</sup>
</italic>
) mice developed neutrophilia, were hypersusceptible to LPS-induced septic shock, and had a high risk of developing spontaneous precursor B cell (pre-B cell) lymphoma with elevated expression of immunosuppressive molecules programmed death ligand 1 (PD-L1) and IL-10. <italic>Becn1</italic>
deficiency resulted in the stabilization of MEKK3 and aberrant p38 activation in neutrophils, and mediated neutrophil–B cell interaction through Cxcl9/Cxcr3 chemotaxis. Neutrophil–B cell interplay further led to the activation of IL-21/STAT3/IRF1 and CD40L/ERK signaling and PD-L1 expression; therefore, it suppressed CD8<sup>+</sup>
T cell function. Ablation of p38 in <italic>Becn1<sup>ΔM</sup>
</italic>
mice prevented neutrophil inflammation and B cell tumorigenesis. Importantly, the low expression of Becn1 in human neutrophils was significantly correlated with the PD-L1 levels in pre-B acute lymphoblastic lymphoma (ALL) patients. Our findings have identified myeloid Becn1 as a key regulator of cancer immunity and therapeutic target for pre-B cell lymphomas.</p>
</div>
</front>
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