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The PDL1-inducible GTPase Arl4d controls T effector function by limiting IL-2 production

Standard

The PDL1-inducible GTPase Arl4d controls T effector function by limiting IL-2 production. / Tolksdorf, Felix; Mikulec, Julita; Geers, Bernd; Endig, Jessica; Sprezyna, Paulina; Heukamp, Lukas C; Knolle, Percy A; Kolanus, Waldemar; Diehl, Linda.

In: SCI REP-UK, Vol. 8, No. 1, 31.10.2018, p. 16123.

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

Harvard

Tolksdorf, F, Mikulec, J, Geers, B, Endig, J, Sprezyna, P, Heukamp, LC, Knolle, PA, Kolanus, W & Diehl, L 2018, 'The PDL1-inducible GTPase Arl4d controls T effector function by limiting IL-2 production', SCI REP-UK, vol. 8, no. 1, pp. 16123. https://doi.org/10.1038/s41598-018-34522-4

APA

Tolksdorf, F., Mikulec, J., Geers, B., Endig, J., Sprezyna, P., Heukamp, L. C., Knolle, P. A., Kolanus, W., & Diehl, L. (2018). The PDL1-inducible GTPase Arl4d controls T effector function by limiting IL-2 production. SCI REP-UK, 8(1), 16123. https://doi.org/10.1038/s41598-018-34522-4

Vancouver

Tolksdorf F, Mikulec J, Geers B, Endig J, Sprezyna P, Heukamp LC et al. The PDL1-inducible GTPase Arl4d controls T effector function by limiting IL-2 production. SCI REP-UK. 2018 Oct 31;8(1):16123. https://doi.org/10.1038/s41598-018-34522-4

Bibtex

@article{5da5c8566d6044f4a6ecc2612680d041,
title = "The PDL1-inducible GTPase Arl4d controls T effector function by limiting IL-2 production",
abstract = "Interleukin-2 (IL-2) is a key regulator of adaptive immune responses but its regulation is incompletely understood. We previously found that PDL1-dependent signals were pivotal for liver sinusoidal endothelial cell-mediated priming of CD8 T cells, which have a strongly reduced capacity to produce IL-2. Here, we show that the expression of the ARF-like GTPase Arl4d is PD-L1-dependently induced in such LSEC-primed T cells, and is associated with reduced IL-2 secretion and Akt phosphorylation. Conversely, Arl4d-deficient T cells overproduced IL-2 upon stimulation. Arl4d-deficiency in CD8 T cells also enhanced their expansion and effector function during viral infection in vivo. Consistent with their increased IL-2 production, Arl4d-deficient T cells showed enhanced development into KLRG1+CD127- short-lived effector cells (SLEC), which is dependent on IL-2 availability. Thus, our data reveal a PD-L1-dependent regulatory circuitry that involves the induction of Arl4d for limiting IL-2 production in T cells.",
keywords = "Journal Article",
author = "Felix Tolksdorf and Julita Mikulec and Bernd Geers and Jessica Endig and Paulina Sprezyna and Heukamp, {Lukas C} and Knolle, {Percy A} and Waldemar Kolanus and Linda Diehl",
year = "2018",
month = oct,
day = "31",
doi = "10.1038/s41598-018-34522-4",
language = "English",
volume = "8",
pages = "16123",
journal = "SCI REP-UK",
issn = "2045-2322",
publisher = "NATURE PUBLISHING GROUP",
number = "1",

}

RIS

TY - JOUR

T1 - The PDL1-inducible GTPase Arl4d controls T effector function by limiting IL-2 production

AU - Tolksdorf, Felix

AU - Mikulec, Julita

AU - Geers, Bernd

AU - Endig, Jessica

AU - Sprezyna, Paulina

AU - Heukamp, Lukas C

AU - Knolle, Percy A

AU - Kolanus, Waldemar

AU - Diehl, Linda

PY - 2018/10/31

Y1 - 2018/10/31

N2 - Interleukin-2 (IL-2) is a key regulator of adaptive immune responses but its regulation is incompletely understood. We previously found that PDL1-dependent signals were pivotal for liver sinusoidal endothelial cell-mediated priming of CD8 T cells, which have a strongly reduced capacity to produce IL-2. Here, we show that the expression of the ARF-like GTPase Arl4d is PD-L1-dependently induced in such LSEC-primed T cells, and is associated with reduced IL-2 secretion and Akt phosphorylation. Conversely, Arl4d-deficient T cells overproduced IL-2 upon stimulation. Arl4d-deficiency in CD8 T cells also enhanced their expansion and effector function during viral infection in vivo. Consistent with their increased IL-2 production, Arl4d-deficient T cells showed enhanced development into KLRG1+CD127- short-lived effector cells (SLEC), which is dependent on IL-2 availability. Thus, our data reveal a PD-L1-dependent regulatory circuitry that involves the induction of Arl4d for limiting IL-2 production in T cells.

AB - Interleukin-2 (IL-2) is a key regulator of adaptive immune responses but its regulation is incompletely understood. We previously found that PDL1-dependent signals were pivotal for liver sinusoidal endothelial cell-mediated priming of CD8 T cells, which have a strongly reduced capacity to produce IL-2. Here, we show that the expression of the ARF-like GTPase Arl4d is PD-L1-dependently induced in such LSEC-primed T cells, and is associated with reduced IL-2 secretion and Akt phosphorylation. Conversely, Arl4d-deficient T cells overproduced IL-2 upon stimulation. Arl4d-deficiency in CD8 T cells also enhanced their expansion and effector function during viral infection in vivo. Consistent with their increased IL-2 production, Arl4d-deficient T cells showed enhanced development into KLRG1+CD127- short-lived effector cells (SLEC), which is dependent on IL-2 availability. Thus, our data reveal a PD-L1-dependent regulatory circuitry that involves the induction of Arl4d for limiting IL-2 production in T cells.

KW - Journal Article

U2 - 10.1038/s41598-018-34522-4

DO - 10.1038/s41598-018-34522-4

M3 - SCORING: Journal article

C2 - 30382149

VL - 8

SP - 16123

JO - SCI REP-UK

JF - SCI REP-UK

SN - 2045-2322

IS - 1

ER -