BATF3 programs CD8+ T cell memory

Ataide MA, Komander K, Knoepper K, Peters AE, Wu H, Eickhoff S, Gogishvili T, Weber J, Grafen A, Kallies A, Garbi N, Einsele H, Hudecek M, Gasteiger G, Hoelzel M, Vaeth M, Kastenmueller W (2020)

Publication Type: Journal article

Publication year: 2020

Journal

Nature Immunology Nature Research

Book Volume: 21

Pages Range: 1397-1407

Journal Issue: 11

DOI: 10.1038/s41590-020-0786-2

Abstract

Antiviral CD8+ T cell responses are characterized by an initial activation/priming of T lymphocytes followed by a massive proliferation, subset differentiation, population contraction and the development of a stable memory pool. The transcription factor BATF3 has been shown to play a central role in the development of conventional dendritic cells, which in turn are critical for optimal priming of CD8+ T cells. Here we show that BATF3 was expressed transiently within the first days after T cell priming and had long-lasting T cell–intrinsic effects. T cells that lacked Batf3 showed normal expansion and differentiation, yet succumbed to an aggravated contraction and had a diminished memory response. Vice versa, BATF3 overexpression in CD8+ T cells promoted their survival and transition to memory. Mechanistically, BATF3 regulated T cell apoptosis and longevity via the proapoptotic factor BIM. By programing CD8+ T cell survival and memory, BATF3 is a promising molecule to optimize adoptive T cell therapy in patients.

Involved external institutions

Julius-Maximilians-Universität Würzburg DE Germany (DE) The University of Melbourne AU Australia (AU) Rheinische Friedrich-Wilhelms-Universität Bonn DE Germany (DE)

How to cite

APA:

Ataide, M.A., Komander, K., Knoepper, K., Peters, A.E., Wu, H., Eickhoff, S.,... Kastenmueller, W. (2020). BATF3 programs CD8+ T cell memory. Nature Immunology, 21(11), 1397-1407. https://doi.org/10.1038/s41590-020-0786-2

MLA:

Ataide, Marco A., et al. "BATF3 programs CD8+ T cell memory." Nature Immunology 21.11 (2020): 1397-1407.

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