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Infectious stimuli promote malignant B-cell acute lymphoblastic leukemia in the absence of AID
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Infectious stimuli promote malignant B-cell acute lymphoblastic leukemia in the absence of AID
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Journal Article
Infectious stimuli promote malignant B-cell acute lymphoblastic leukemia in the absence of AID
2019
Overview
The prerequisite to prevent childhood B-cell acute lymphoblastic leukemia (B-ALL) is to decipher its etiology. The current model suggests that infection triggers B-ALL development through induction of activation-induced cytidine deaminase (AID; also known as AICDA) in precursor B-cells. This evidence has been largely acquired through the use of
ex vivo
functional studies. However, whether this mechanism governs native non-transplant B-ALL development is unknown. Here we show that, surprisingly, AID genetic deletion does not affect B-ALL development in Pax5-haploinsufficient mice prone to B-ALL upon natural infection exposure. We next test the effect of premature AID expression from earliest pro-B-cell stages in B-cell transformation. The generation of AID off-target mutagenic activity in precursor B-cells does not promote B-ALL. Likewise, known drivers of human B-ALL are not preferentially targeted by AID. Overall these results suggest that infections promote B-ALL through AID-independent mechanisms, providing evidence for a new model of childhood B-ALL development.
Infection or chronic inflammation is a risk factor for childhood B-cell precursor acute lymphoblastic leukemia. Here, the authors show that the DNA editing enzyme AID is expressed in infected B cells but using genetic mouse models show that it does not contribute to leukemia pathogenesis.
Publisher
Nature Publishing Group UK,Nature Publishing Group,Nature Portfolio
Subject
/ 38/22
/ 38/23
/ 38/61
/ 38/77
/ 38/90
/ 45
/ 45/23
/ 64
/ 64/60
/ Activation-induced cytidine deaminase
/ Acute lymphoblastic leukemia
/ Animals
/ Cell Transformation, Neoplastic - genetics
/ Cell Transformation, Neoplastic - metabolism
/ Child
/ Children
/ Cytidine Deaminase - genetics
/ Cytidine Deaminase - metabolism
/ Etiology
/ Gene Expression Regulation, Neoplastic
/ High-Throughput Nucleotide Sequencing - methods
/ Humanities and Social Sciences
/ Humans
/ Infections - physiopathology
/ Leukemia
/ PAX5 Transcription Factor - genetics
/ PAX5 Transcription Factor - metabolism
/ Precursor B-Cell Lymphoblastic Leukemia-Lymphoma - genetics
/ Precursor B-Cell Lymphoblastic Leukemia-Lymphoma - metabolism
/ Science
