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Interferon regulatory factor 4 controls effector functions of CD8+ memory T cells

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Interferon regulatory factor 4 controls effector functions of CD8+ memory T cells. / Harberts, Aenne; Schmidt, Constantin; Schmid, Joanna; Reimers, Daniel; Koch-Nolte, Friedrich; Mittrücker, Hans-Willi; Raczkowski, Friederike.

In: P NATL ACAD SCI USA, Vol. 118, No. 16, 20.04.2021, p. e2014553118.

Research output: SCORING: Contribution to journal › SCORING: Journal article › Research › peer-review

Harvard

Harberts, A, Schmidt, C, Schmid, J, Reimers, D, Koch-Nolte, F, Mittrücker, H-W & Raczkowski, F 2021, 'Interferon regulatory factor 4 controls effector functions of CD8+ memory T cells', P NATL ACAD SCI USA, vol. 118, no. 16, pp. e2014553118. https://doi.org/10.1073/pnas.2014553118

APA

Harberts, A., Schmidt, C., Schmid, J., Reimers, D., Koch-Nolte, F., Mittrücker, H-W., & Raczkowski, F. (2021). Interferon regulatory factor 4 controls effector functions of CD8+ memory T cells. P NATL ACAD SCI USA, 118(16), e2014553118. https://doi.org/10.1073/pnas.2014553118

Vancouver

Harberts A, Schmidt C, Schmid J, Reimers D, Koch-Nolte F, Mittrücker H-W et al. Interferon regulatory factor 4 controls effector functions of CD8+ memory T cells. P NATL ACAD SCI USA. 2021 Apr 20;118(16):e2014553118. https://doi.org/10.1073/pnas.2014553118

Bibtex

@article{d5a31621097948ba8fa0b67b0912499c,
title = "Interferon regulatory factor 4 controls effector functions of CD8+ memory T cells",
abstract = "The transcription factor IRF4 is required for CD8+ T cell activation, proliferation, and differentiation to effector cells and thus is essential for robust CD8+ T cell responses. The function of IRF4 in memory CD8+ T cells yet needs to be explored. To investigate the role of IRF4 for maintaining differentiation state and survival of CD8+ memory T cells, we used a mouse model with tamoxifen-inducible Irf4 knockout to preclude effects due to inefficient memory cell differentiation in absence of IRF4. We infected mice with ovalbumin-recombinant listeria and induced Irf4 knockout after clearance of the pathogen. Loss of IRF4 resulted in phenotypical changes of CD8+ memory T cells but did not cause a reduction of the total memory T cell population. However, upon reencounter of the pathogen, CD8+ memory T cells showed impaired expansion and acquisition of effector functions. When compared to CD8+ effector memory T cells, CD8+ tissue-resident memory T cells (TRM cells) expressed higher IRF4 levels. Mice with constitutive Irf4 knockout had diminished CD8+ TRM-cell populations, and tamoxifen-induced Irf4 deletion caused a reduction of this cell population. In conclusion, our results demonstrate that IRF4 is required for effective reactivation but not for general survival of CD8+ memory T cells. Formation and maintenance of CD8+ TRM cells, in contrast, appear to depend on IRF4.",
author = "Aenne Harberts and Constantin Schmidt and Joanna Schmid and Daniel Reimers and Friedrich Koch-Nolte and Hans-Willi Mittr{\"u}cker and Friederike Raczkowski",
year = "2021",
month = apr,
day = "20",
doi = "10.1073/pnas.2014553118",
language = "English",
volume = "118",
pages = "e2014553118",
journal = "P NATL ACAD SCI USA",
issn = "0027-8424",
publisher = "National Academy of Sciences",
number = "16",

}

RIS

TY - JOUR

T1 - Interferon regulatory factor 4 controls effector functions of CD8+ memory T cells

AU - Harberts, Aenne

AU - Schmidt, Constantin

AU - Schmid, Joanna

AU - Reimers, Daniel

AU - Koch-Nolte, Friedrich

AU - Mittrücker, Hans-Willi

AU - Raczkowski, Friederike

PY - 2021/4/20

Y1 - 2021/4/20

N2 - The transcription factor IRF4 is required for CD8+ T cell activation, proliferation, and differentiation to effector cells and thus is essential for robust CD8+ T cell responses. The function of IRF4 in memory CD8+ T cells yet needs to be explored. To investigate the role of IRF4 for maintaining differentiation state and survival of CD8+ memory T cells, we used a mouse model with tamoxifen-inducible Irf4 knockout to preclude effects due to inefficient memory cell differentiation in absence of IRF4. We infected mice with ovalbumin-recombinant listeria and induced Irf4 knockout after clearance of the pathogen. Loss of IRF4 resulted in phenotypical changes of CD8+ memory T cells but did not cause a reduction of the total memory T cell population. However, upon reencounter of the pathogen, CD8+ memory T cells showed impaired expansion and acquisition of effector functions. When compared to CD8+ effector memory T cells, CD8+ tissue-resident memory T cells (TRM cells) expressed higher IRF4 levels. Mice with constitutive Irf4 knockout had diminished CD8+ TRM-cell populations, and tamoxifen-induced Irf4 deletion caused a reduction of this cell population. In conclusion, our results demonstrate that IRF4 is required for effective reactivation but not for general survival of CD8+ memory T cells. Formation and maintenance of CD8+ TRM cells, in contrast, appear to depend on IRF4.

AB - The transcription factor IRF4 is required for CD8+ T cell activation, proliferation, and differentiation to effector cells and thus is essential for robust CD8+ T cell responses. The function of IRF4 in memory CD8+ T cells yet needs to be explored. To investigate the role of IRF4 for maintaining differentiation state and survival of CD8+ memory T cells, we used a mouse model with tamoxifen-inducible Irf4 knockout to preclude effects due to inefficient memory cell differentiation in absence of IRF4. We infected mice with ovalbumin-recombinant listeria and induced Irf4 knockout after clearance of the pathogen. Loss of IRF4 resulted in phenotypical changes of CD8+ memory T cells but did not cause a reduction of the total memory T cell population. However, upon reencounter of the pathogen, CD8+ memory T cells showed impaired expansion and acquisition of effector functions. When compared to CD8+ effector memory T cells, CD8+ tissue-resident memory T cells (TRM cells) expressed higher IRF4 levels. Mice with constitutive Irf4 knockout had diminished CD8+ TRM-cell populations, and tamoxifen-induced Irf4 deletion caused a reduction of this cell population. In conclusion, our results demonstrate that IRF4 is required for effective reactivation but not for general survival of CD8+ memory T cells. Formation and maintenance of CD8+ TRM cells, in contrast, appear to depend on IRF4.

U2 - 10.1073/pnas.2014553118

DO - 10.1073/pnas.2014553118

M3 - SCORING: Journal article

C2 - 33859042

VL - 118

SP - e2014553118

JO - P NATL ACAD SCI USA

JF - P NATL ACAD SCI USA

SN - 0027-8424

IS - 16

ER -