ChloroquineV1, Main, Exploration, bibRecord, 004007

Myeloid loss of Beclin 1 promotes PD-L1hi precursor B cell lymphoma development

Identifieur interne : 004007 ( Main/Exploration ); précédent : 004006; suivant : 004008

Myeloid 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 ] ; ????.

RBID : PMC:6877338

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 Becn1 (Becn1^ΔM) 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. Becn1 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⁺ T cell function. Ablation of p38 in Becn1^ΔM 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.

Url:

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6877338

DOI: 10.1172/JCI127721
PubMed: 31503548
PubMed Central: 6877338

Affiliations:

Le document en format XML

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 promotes PD-L1<sup>hi</sup>
 precursor B cell lymphoma development</title>
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 promotes PD-L1<sup>hi</sup>
 precursor B cell lymphoma development</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>
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<name sortKey="Wang, Rong Fu" sort="Wang, Rong Fu" uniqKey="Wang R" first="Rong-Fu" last="Wang">Rong-Fu Wang</name>
<name sortKey="Xing, Changsheng" sort="Xing, Changsheng" uniqKey="Xing C" first="Changsheng" last="Xing">Changsheng Xing</name>
<name sortKey="You, M James" sort="You, M James" uniqKey="You M" first="M. James" last="You">M. James You</name>
<name sortKey="Yu, Xiao" sort="Yu, Xiao" uniqKey="Yu X" first="Xiao" last="Yu">Xiao Yu</name>
<name sortKey="Zhou, Yubin" sort="Zhou, Yubin" uniqKey="Zhou Y" first="Yubin" last="Zhou">Yubin Zhou</name>
<name sortKey="Zhu, Motao" sort="Zhu, Motao" uniqKey="Zhu M" first="Motao" last="Zhu">Motao Zhu</name>
</country>
<country name="République populaire de Chine"><noRegion><name sortKey="Mao, Jingrong" sort="Mao, Jingrong" uniqKey="Mao J" first="Jingrong" last="Mao">Jingrong Mao</name>
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</affiliations>
</record>

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{{Explor lien
   |wiki=    Sante
   |area=    ChloroquineV1
   |flux=    Main
   |étape=   Exploration
   |type=    RBID
   |clé=     PMC:6877338
   |texte=   Myeloid loss of Beclin 1 promotes PD-L1hi precursor B cell lymphoma development
}}

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Serveur d'exploration Chloroquine

Myeloid loss of Beclin 1 promotes PD-L1hi precursor B cell lymphoma development

Myeloid loss of Beclin 1 promotes PD-L1hi precursor B cell lymphoma development

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Abstract

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	Serveur d'exploration Chloroquine
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