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The ADP-Ribosylation Factor 4d Restricts Regulatory T-Cell Induction via Control of IL-2 Availability

Standard

The ADP-Ribosylation Factor 4d Restricts Regulatory T-Cell Induction via Control of IL-2 Availability. / Geers, Bernd; Hagenstein, Julia; Endig, Jessica; Ulrich, Hanna; Fleig, Laura; Sprezyna, Paulina; Mikulec, Julita; Heukamp, Lukas; Tiegs, Gisa; Diehl, Linda.

In: CELLS-BASEL, Vol. 11, No. 17, 2639, 25.08.2022.

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

Harvard

Geers, B, Hagenstein, J, Endig, J, Ulrich, H, Fleig, L, Sprezyna, P, Mikulec, J, Heukamp, L, Tiegs, G & Diehl, L 2022, 'The ADP-Ribosylation Factor 4d Restricts Regulatory T-Cell Induction via Control of IL-2 Availability', CELLS-BASEL, vol. 11, no. 17, 2639. https://doi.org/10.3390/cells11172639

APA

Geers, B., Hagenstein, J., Endig, J., Ulrich, H., Fleig, L., Sprezyna, P., Mikulec, J., Heukamp, L., Tiegs, G., & Diehl, L. (2022). The ADP-Ribosylation Factor 4d Restricts Regulatory T-Cell Induction via Control of IL-2 Availability. CELLS-BASEL, 11(17), [2639]. https://doi.org/10.3390/cells11172639

Vancouver

Geers B, Hagenstein J, Endig J, Ulrich H, Fleig L, Sprezyna P et al. The ADP-Ribosylation Factor 4d Restricts Regulatory T-Cell Induction via Control of IL-2 Availability. CELLS-BASEL. 2022 Aug 25;11(17). 2639. https://doi.org/10.3390/cells11172639

Bibtex

@article{b99fe4f5352d43558dcfccea3d75286a,
title = "The ADP-Ribosylation Factor 4d Restricts Regulatory T-Cell Induction via Control of IL-2 Availability",
abstract = "Interleukin-2 is central to the induction and maintenance of both natural (nTreg) and induced Foxp3-expressing regulatory T cells (iTreg). Thus, signals that modulate IL-2 availability may, in turn, also influence Treg homeostasis. Using global knockout and cell-specific knockout mouse models, we evaluated the role of the small GTPase ADP-ribosylation factor 4d (Arl4d) in regulatory T-cell biology. We show that the expression of Arl4d in T cells restricts both IL-2 production and responsiveness to IL-2, as measured by the phosphorylation of STAT5. Arl4d-deficient CD4 T cells converted more efficiently into Foxp3+ iTreg in vitro in the presence of αCD3ε and TGFβ, which was associated with their enhanced IL-2 secretion. As such, Arl4d-/- CD4 T cells induced significantly less colonic inflammation and lymphocytic infiltration in a model of transfer colitis. Thus, our data reveal a negative regulatory role for Arl4d in CD4 T-cell biology, limiting iTreg conversion via the restriction of IL-2 production, leading to reduced induction of Treg from conventional CD4 T cells.",
author = "Bernd Geers and Julia Hagenstein and Jessica Endig and Hanna Ulrich and Laura Fleig and Paulina Sprezyna and Julita Mikulec and Lukas Heukamp and Gisa Tiegs and Linda Diehl",
year = "2022",
month = aug,
day = "25",
doi = "10.3390/cells11172639",
language = "English",
volume = "11",
journal = "CELLS-BASEL",
issn = "2073-4409",
publisher = "MDPI Multidisciplinary Digital Publishing Institute",
number = "17",

}

RIS

TY - JOUR

T1 - The ADP-Ribosylation Factor 4d Restricts Regulatory T-Cell Induction via Control of IL-2 Availability

AU - Geers, Bernd

AU - Hagenstein, Julia

AU - Endig, Jessica

AU - Ulrich, Hanna

AU - Fleig, Laura

AU - Sprezyna, Paulina

AU - Mikulec, Julita

AU - Heukamp, Lukas

AU - Tiegs, Gisa

AU - Diehl, Linda

PY - 2022/8/25

Y1 - 2022/8/25

N2 - Interleukin-2 is central to the induction and maintenance of both natural (nTreg) and induced Foxp3-expressing regulatory T cells (iTreg). Thus, signals that modulate IL-2 availability may, in turn, also influence Treg homeostasis. Using global knockout and cell-specific knockout mouse models, we evaluated the role of the small GTPase ADP-ribosylation factor 4d (Arl4d) in regulatory T-cell biology. We show that the expression of Arl4d in T cells restricts both IL-2 production and responsiveness to IL-2, as measured by the phosphorylation of STAT5. Arl4d-deficient CD4 T cells converted more efficiently into Foxp3+ iTreg in vitro in the presence of αCD3ε and TGFβ, which was associated with their enhanced IL-2 secretion. As such, Arl4d-/- CD4 T cells induced significantly less colonic inflammation and lymphocytic infiltration in a model of transfer colitis. Thus, our data reveal a negative regulatory role for Arl4d in CD4 T-cell biology, limiting iTreg conversion via the restriction of IL-2 production, leading to reduced induction of Treg from conventional CD4 T cells.

AB - Interleukin-2 is central to the induction and maintenance of both natural (nTreg) and induced Foxp3-expressing regulatory T cells (iTreg). Thus, signals that modulate IL-2 availability may, in turn, also influence Treg homeostasis. Using global knockout and cell-specific knockout mouse models, we evaluated the role of the small GTPase ADP-ribosylation factor 4d (Arl4d) in regulatory T-cell biology. We show that the expression of Arl4d in T cells restricts both IL-2 production and responsiveness to IL-2, as measured by the phosphorylation of STAT5. Arl4d-deficient CD4 T cells converted more efficiently into Foxp3+ iTreg in vitro in the presence of αCD3ε and TGFβ, which was associated with their enhanced IL-2 secretion. As such, Arl4d-/- CD4 T cells induced significantly less colonic inflammation and lymphocytic infiltration in a model of transfer colitis. Thus, our data reveal a negative regulatory role for Arl4d in CD4 T-cell biology, limiting iTreg conversion via the restriction of IL-2 production, leading to reduced induction of Treg from conventional CD4 T cells.

U2 - 10.3390/cells11172639

DO - 10.3390/cells11172639

M3 - SCORING: Journal article

C2 - 36078047

VL - 11

JO - CELLS-BASEL

JF - CELLS-BASEL

SN - 2073-4409

IS - 17

M1 - 2639

ER -