MicroRNA 10a marks regulatory T cells

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MicroRNA 10a marks regulatory T cells. / Jeker, Lukas T; Zhou, Xuyu; Gershberg, Kseniya; de Kouchkovsky, Dimitri; Morar, Malika M; Stadthagen, Gustavo; Lund, Anders H.; Bluestone, Jeffrey A.

In: PLOS ONE, Vol. 7, No. 5, 2012, p. e36684.

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

Harvard

Jeker, LT, Zhou, X, Gershberg, K, de Kouchkovsky, D, Morar, MM, Stadthagen, G, Lund, AH & Bluestone, JA 2012, 'MicroRNA 10a marks regulatory T cells', PLOS ONE, vol. 7, no. 5, pp. e36684. https://doi.org/10.1371/journal.pone.0036684

APA

Jeker, L. T., Zhou, X., Gershberg, K., de Kouchkovsky, D., Morar, M. M., Stadthagen, G., Lund, A. H., & Bluestone, J. A. (2012). MicroRNA 10a marks regulatory T cells. PLOS ONE, 7(5), e36684. https://doi.org/10.1371/journal.pone.0036684

Vancouver

Jeker LT, Zhou X, Gershberg K, de Kouchkovsky D, Morar MM, Stadthagen G et al. MicroRNA 10a marks regulatory T cells. PLOS ONE. 2012;7(5):e36684. https://doi.org/10.1371/journal.pone.0036684

Author

Jeker, Lukas T ; Zhou, Xuyu ; Gershberg, Kseniya ; de Kouchkovsky, Dimitri ; Morar, Malika M ; Stadthagen, Gustavo ; Lund, Anders H. ; Bluestone, Jeffrey A. / MicroRNA 10a marks regulatory T cells. In: PLOS ONE. 2012 ; Vol. 7, No. 5. pp. e36684.

Bibtex

@article{125371cad2bf40b7b0da8cb367d39d5d,
title = "MicroRNA 10a marks regulatory T cells",
abstract = "MicroRNAs (miRNAs) are crucial for regulatory T cell (Treg) stability and function. We report that microRNA-10a (miR-10a) is expressed in Tregs but not in other T cells including individual thymocyte subsets. Expression profiling in inbred mouse strains demonstrated that non-obese diabetic (NOD) mice with a genetic susceptibility for autoimmune diabetes have lower Treg-specific miR-10a expression than C57BL/6J autoimmune resistant mice. Inhibition of miR-10a expression in vitro leads to reduced FoxP3 expression levels and miR-10a expression is lower in unstable {"}exFoxP3{"} T cells. Unstable in vitro TGF-{\ss}-induced, iTregs do not express miR-10a unless cultured in the presence of retinoic acid (RA) which has been associated with increased stability of iTreg, suggesting that miR-10a might play a role in stabilizing Treg. However, genetic ablation of miR-10a neither affected the number and phenotype of natural Treg nor the capacity of conventional T cells to induce FoxP3 in response to TGFβ, RA, or a combination of the two. Thus, miR-10a is selectively expressed in Treg but inhibition by antagomiRs or genetic ablation resulted in discordant effects on FoxP3.",
keywords = "Animals, Cells, Cultured, Diabetes Mellitus, Type 1, Gene Expression, Mice, Mice, Inbred NOD, MicroRNAs, T-Lymphocytes, Regulatory, Transforming Growth Factor beta, Tretinoin",
author = "Jeker, {Lukas T} and Xuyu Zhou and Kseniya Gershberg and {de Kouchkovsky}, Dimitri and Morar, {Malika M} and Gustavo Stadthagen and Lund, {Anders H.} and Bluestone, {Jeffrey A}",
year = "2012",
doi = "10.1371/journal.pone.0036684",
language = "English",
volume = "7",
pages = "e36684",
journal = "PLoS ONE",
issn = "1932-6203",
publisher = "Public Library of Science",
number = "5",

}

RIS

TY - JOUR

T1 - MicroRNA 10a marks regulatory T cells

AU - Jeker, Lukas T

AU - Zhou, Xuyu

AU - Gershberg, Kseniya

AU - de Kouchkovsky, Dimitri

AU - Morar, Malika M

AU - Stadthagen, Gustavo

AU - Lund, Anders H.

AU - Bluestone, Jeffrey A

PY - 2012

Y1 - 2012

N2 - MicroRNAs (miRNAs) are crucial for regulatory T cell (Treg) stability and function. We report that microRNA-10a (miR-10a) is expressed in Tregs but not in other T cells including individual thymocyte subsets. Expression profiling in inbred mouse strains demonstrated that non-obese diabetic (NOD) mice with a genetic susceptibility for autoimmune diabetes have lower Treg-specific miR-10a expression than C57BL/6J autoimmune resistant mice. Inhibition of miR-10a expression in vitro leads to reduced FoxP3 expression levels and miR-10a expression is lower in unstable "exFoxP3" T cells. Unstable in vitro TGF-ß-induced, iTregs do not express miR-10a unless cultured in the presence of retinoic acid (RA) which has been associated with increased stability of iTreg, suggesting that miR-10a might play a role in stabilizing Treg. However, genetic ablation of miR-10a neither affected the number and phenotype of natural Treg nor the capacity of conventional T cells to induce FoxP3 in response to TGFβ, RA, or a combination of the two. Thus, miR-10a is selectively expressed in Treg but inhibition by antagomiRs or genetic ablation resulted in discordant effects on FoxP3.

AB - MicroRNAs (miRNAs) are crucial for regulatory T cell (Treg) stability and function. We report that microRNA-10a (miR-10a) is expressed in Tregs but not in other T cells including individual thymocyte subsets. Expression profiling in inbred mouse strains demonstrated that non-obese diabetic (NOD) mice with a genetic susceptibility for autoimmune diabetes have lower Treg-specific miR-10a expression than C57BL/6J autoimmune resistant mice. Inhibition of miR-10a expression in vitro leads to reduced FoxP3 expression levels and miR-10a expression is lower in unstable "exFoxP3" T cells. Unstable in vitro TGF-ß-induced, iTregs do not express miR-10a unless cultured in the presence of retinoic acid (RA) which has been associated with increased stability of iTreg, suggesting that miR-10a might play a role in stabilizing Treg. However, genetic ablation of miR-10a neither affected the number and phenotype of natural Treg nor the capacity of conventional T cells to induce FoxP3 in response to TGFβ, RA, or a combination of the two. Thus, miR-10a is selectively expressed in Treg but inhibition by antagomiRs or genetic ablation resulted in discordant effects on FoxP3.

KW - Animals

KW - Cells, Cultured

KW - Diabetes Mellitus, Type 1

KW - Gene Expression

KW - Mice

KW - Mice, Inbred NOD

KW - MicroRNAs

KW - T-Lymphocytes, Regulatory

KW - Transforming Growth Factor beta

KW - Tretinoin

U2 - 10.1371/journal.pone.0036684

DO - 10.1371/journal.pone.0036684

M3 - Journal article

C2 - 22629323

VL - 7

SP - e36684

JO - PLoS ONE

JF - PLoS ONE

SN - 1932-6203

IS - 5

ER -

ID: 50503769