An evolved AAV variant enables efficient genetic engineering of murine T cells

William A. Nyberg(Gladstone Institutes), Jonathan Ark(Duke University), Angela To(Gladstone Institutes), Sylvanie Clouden(Duke University), Gabriella C. Reeder(Gladstone Institutes), Joseph J. Muldoon(Gladstone Institutes), Jing-Yi Chung(Gladstone Institutes), William Xie(University of California, San Francisco), Vincent Allain(Gladstone Institutes), Zachary Steinhart(Gladstone Institutes), Christopher Chang(Gladstone Institutes), Alexis Talbot(Gladstone Institutes), Sandy Kim(University of California, Los Angeles), Alan Rosales(Duke University), L. Patrick Havlik(Duke University), Harold Pimentel(Howard Hughes Medical Institute), Aravind Asokan(Duke University), Justin Eyquem(Gladstone Institutes)
Cell
January 1, 2023
Cited by 90Open Access
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Abstract

Precise targeting of large transgenes to T cells using homology-directed repair has been transformative for adoptive cell therapies and T cell biology. Delivery of DNA templates via adeno-associated virus (AAV) has greatly improved knockin efficiencies, but the tropism of current AAV serotypes restricts their use to human T cells employed in immunodeficient mouse models. To enable targeted knockins in murine T cells, we evolved Ark313, a synthetic AAV that exhibits high transduction efficiency in murine T cells. We performed a genome-wide knockout screen and identified QA2 as an essential factor for Ark313 infection. We demonstrate that Ark313 can be used for nucleofection-free DNA delivery, CRISPR-Cas9-mediated knockouts, and targeted integration of large transgenes. Ark313 enables preclinical modeling of Trac-targeted CAR-T and transgenic TCR-T cells in immunocompetent models. Efficient gene targeting in murine T cells holds great potential for improved cell therapies and opens avenues in experimental T cell immunology.


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