Optimal Avidity of the Immune Synapse and Mitochondrial Repair Trigger Asymmetrical Cell Division and CAR T Cell Persistence - Review.
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TL;DR
A hypothesis linking mitophagy to CAR T cell exhaustion is presented, modulation of which may be clinically relevant in the treatment of cancers with CAR T cells.
OpenAlex 토픽 ·
CAR-T cell therapy research
Cancer Immunotherapy and Biomarkers
Immunotherapy and Immune Responses
A hypothesis linking mitophagy to CAR T cell exhaustion is presented, modulation of which may be clinically relevant in the treatment of cancers with CAR T cells.
APA
Jyotishankar Raychaudhuri, Claudio Anasetti (2026). Optimal Avidity of the Immune Synapse and Mitochondrial Repair Trigger Asymmetrical Cell Division and CAR T Cell Persistence - Review.. Transplantation and cellular therapy, 32(4), 398-411. https://doi.org/10.1016/j.jtct.2025.12.988
MLA
Jyotishankar Raychaudhuri, et al.. "Optimal Avidity of the Immune Synapse and Mitochondrial Repair Trigger Asymmetrical Cell Division and CAR T Cell Persistence - Review.." Transplantation and cellular therapy, vol. 32, no. 4, 2026, pp. 398-411.
PMID
41455592 ↗
Abstract 한글 요약
Chimeric antigen receptor (CAR) T cell persistence with memory is the current research focus of cancer immunotherapy. The incomplete effect of CAR T cells against tumors results from CAR T cell dysfunction and exhaustion. Asymmetric cell division is an evolutionarily conserved mechanism to maintain mother stem cells during embryonic development, and for immune cells to provide a continuous supply of diverse populations to fight infections and cancer. CAR T cells use ACD to determine their fate during the first mitotic division after interaction with its target, creating a pool of memory CAR T cells which can be recalled to be effector cells during tumor relapse, necessarily to offset the diminished ability of exhausted CAR T cells in controlling the tumor. Affinity of the CAR T - target cell immune synapse and mitochondrial dynamics regulate ACD. We review the literature regarding CAR T cell persistence, exhaustion, and mechanisms of reversing exhaustion. Subsequently, we present a hypothesis linking mitophagy to CAR T cell exhaustion, modulation of which may be clinically relevant in the treatment of cancers with CAR T cells.
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