MINI REVIEW article
Front. Immunol.
Sec. Cancer Immunity and Immunotherapy
Volume 16 - 2025 | doi: 10.3389/fimmu.2025.1531145
This article is part of the Research TopicDissecting the Role of T Cell Exhaustion in Cancer Progression: A Multifaceted ApproachView all 4 articles
T Cell Exhaustion in Pediatric B-ALL: Current Knowledge and Future Perspectives
Provisionally accepted
- 1Michael Cuccione Childhood Cancer Research Program, BC Children's Hospital Research Institute, Vancouver, Canada
- 2Department of Pediatrics, University of British Columbia, Vancouver, British Columbia, Canada
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B-cell acute lymphoblastic leukemia (B-ALL) is the most common pediatric malignancy, accounting for 20-25% of all new cancer diagnoses in North American children each year. The leukemia arises, most commonly after a latency of 3-5 years, from a preleukemic B cell precursor population generated in utero. Despite the generally low immunogenicity of B-ALL cells, emerging evidence implicates T cell exhaustion -a state marked by sustained expression of inhibitory receptors and progressive functional decline -as a contributor to disease progression. Expression of inhibitory receptors is frequently detected on T cells from children with B-ALL at diagnosis and during therapy. As T cell exhaustion presents an actionable target for enhancing protective immune activity, in this review we summarise evidence from both clinical and pre-clinical settings for T cell exhaustion during pediatric B-ALL progression and discuss the opportunities and challenges to incorporating immune checkpoint blockade into pediatric B-ALL therapy regimens.
Keywords: pediatric B cell precursor acute lymphoblastic leukemia, T cell exhaustion (Tex), Bispecific T cell engager (BiTE), Chimeric antigen receptor (CAR T), immune checkpoint inhibition
Received: 19 Nov 2024; Accepted: 12 May 2025.
Copyright: © 2025 Atre and Reid. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
* Correspondence: Gregor S.D Reid, Michael Cuccione Childhood Cancer Research Program, BC Children's Hospital Research Institute, Vancouver, Canada
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