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Gfi1 controls the formation of effector-like CD8+ T cells during chronic infection and cancer

Oluwagbemiga A. Ojo, Hongxing Shen, Jennifer T. Ingram, James A. Bonner, Robert S. Welner, Georges Lacaud, Allan J. Zajac and Lewis Z. Shi ()
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Oluwagbemiga A. Ojo: University of Alabama at Birmingham
Hongxing Shen: University of Alabama at Birmingham
Jennifer T. Ingram: University of Alabama at Birmingham
James A. Bonner: University of Alabama at Birmingham
Robert S. Welner: University of Alabama at Birmingham
Georges Lacaud: The University of Manchester
Allan J. Zajac: University of Alabama at Birmingham
Lewis Z. Shi: University of Alabama at Birmingham

Nature Communications, 2025, vol. 16, issue 1, 1-18

Abstract: Abstract During chronic infection and tumor progression, CD8+ T cells lose their effector functions and become exhausted. These exhausted CD8+ T cells are heterogeneous and comprised of progenitors that give rise to effector-like or terminally-exhausted cells. The precise cues and mechanisms directing subset formation are incompletely understood. Here, we show that growth factor independent-1 (Gfi1) is dynamically regulated in exhausted CD8+ T cells. During chronic LCMV Clone 13 infection, a previously under-described Ly108+CX3CR1+ subset expresses low levels of Gfi1 while other established subsets have high expression. Ly108+CX3CR1+ cells possess distinct chromatin profiles and represent a transitory subset that develops to effector-like and terminally-exhausted cells, a process dependent on Gfi1. Similarly, Gfi1 in tumor-infiltrating CD8+ T cells is required for the formation of terminally differentiated cells and endogenous as well as anti-CTLA-induced anti-tumor responses. Taken together, Gfi1 is a key regulator of the subset formation of exhausted CD8+ T cells.

Date: 2025
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DOI: 10.1038/s41467-025-59784-1

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