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MiR-125a targets effector programs to stabilize Treg-mediated immune homeostasis

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MiR-125a targets effector programs to stabilize Treg-mediated immune homeostasis. / Pan, Wen; Zhu, Shu; Dai, Dai; Liu, Zheng; Li, Dan; Li, Bin; Gagliani, Nicola; Zheng, Yunjiang; Tang, Yuanjia; Weirauch, Matthew T; Chen, Xiaoting; Zhu, Wei; Wang, Yue; Chen, Bo; Qian, Youcun; Chen, Yingxuan; Fang, Jingyuan; Herbst, Ronald; Richman, Laura; Jallal, Bahija; Harley, John B; Flavell, Richard A; Yao, Yihong; Shen, Nan.

in: NAT COMMUN, Jahrgang 6, 12.05.2015, S. 7096.

Publikationen: SCORING: Beitrag in Fachzeitschrift/Zeitung › SCORING: Zeitschriftenaufsatz › Forschung › Begutachtung

Harvard

Pan, W, Zhu, S, Dai, D, Liu, Z, Li, D, Li, B, Gagliani, N, Zheng, Y, Tang, Y, Weirauch, MT, Chen, X, Zhu, W, Wang, Y, Chen, B, Qian, Y, Chen, Y, Fang, J, Herbst, R, Richman, L, Jallal, B, Harley, JB, Flavell, RA, Yao, Y & Shen, N 2015, 'MiR-125a targets effector programs to stabilize Treg-mediated immune homeostasis', NAT COMMUN, Jg. 6, S. 7096. https://doi.org/10.1038/ncomms8096

APA

Pan, W., Zhu, S., Dai, D., Liu, Z., Li, D., Li, B., Gagliani, N., Zheng, Y., Tang, Y., Weirauch, M. T., Chen, X., Zhu, W., Wang, Y., Chen, B., Qian, Y., Chen, Y., Fang, J., Herbst, R., Richman, L., ... Shen, N. (2015). MiR-125a targets effector programs to stabilize Treg-mediated immune homeostasis. NAT COMMUN, 6, 7096. https://doi.org/10.1038/ncomms8096

Vancouver

Pan W, Zhu S, Dai D, Liu Z, Li D, Li B et al. MiR-125a targets effector programs to stabilize Treg-mediated immune homeostasis. NAT COMMUN. 2015 Mai 12;6:7096. https://doi.org/10.1038/ncomms8096

Bibtex

@article{f1d3714d7f164421b804e92aad78539e,
title = "MiR-125a targets effector programs to stabilize Treg-mediated immune homeostasis",
abstract = "Although different autoimmune diseases show discrete clinical features, there are common molecular pathways intimately involved. Here we show that miR-125a is downregulated in peripheral CD4(+) T cells of human autoimmune diseases including systemic lupus erythematosus and Crohn's disease, and relevant autoimmune mouse models. miR-125a stabilizes both the commitment and immunoregulatory capacity of Treg cells. In miR-125a-deficient mice, the balance appears to shift from immune suppression to inflammation, and results in more severe pathogenesis of colitis and experimental autoimmune encephalomyelitis (EAE). The genome-wide target analysis reveals that miR-125a suppresses several effector T-cell factors including Stat3, Ifng and Il13. Using a chemically synthesized miR-125a analogue, we show potential to re-programme the immune homeostasis in EAE models. These findings point to miR-125a as a critical factor that controls autoimmune diseases by stabilizing Treg-mediated immune homeostasis.",
keywords = "Animals, Case-Control Studies, Colitis, Crohn Disease, Down-Regulation, Homeodomain Proteins, Homeostasis, Humans, Immunity, Cellular, Lupus Erythematosus, Systemic, Mice, Mice, Inbred C57BL, MicroRNAs, Neuritis, Autoimmune, Experimental, T-Lymphocytes, Regulatory, Journal Article, Research Support, Non-U.S. Gov't",
author = "Wen Pan and Shu Zhu and Dai Dai and Zheng Liu and Dan Li and Bin Li and Nicola Gagliani and Yunjiang Zheng and Yuanjia Tang and Weirauch, {Matthew T} and Xiaoting Chen and Wei Zhu and Yue Wang and Bo Chen and Youcun Qian and Yingxuan Chen and Jingyuan Fang and Ronald Herbst and Laura Richman and Bahija Jallal and Harley, {John B} and Flavell, {Richard A} and Yihong Yao and Nan Shen",
year = "2015",
month = may,
day = "12",
doi = "10.1038/ncomms8096",
language = "English",
volume = "6",
pages = "7096",
journal = "NAT COMMUN",
issn = "2041-1723",
publisher = "NATURE PUBLISHING GROUP",

}

RIS

TY - JOUR

T1 - MiR-125a targets effector programs to stabilize Treg-mediated immune homeostasis

AU - Pan, Wen

AU - Zhu, Shu

AU - Dai, Dai

AU - Liu, Zheng

AU - Li, Dan

AU - Li, Bin

AU - Gagliani, Nicola

AU - Zheng, Yunjiang

AU - Tang, Yuanjia

AU - Weirauch, Matthew T

AU - Chen, Xiaoting

AU - Zhu, Wei

AU - Wang, Yue

AU - Chen, Bo

AU - Qian, Youcun

AU - Chen, Yingxuan

AU - Fang, Jingyuan

AU - Herbst, Ronald

AU - Richman, Laura

AU - Jallal, Bahija

AU - Harley, John B

AU - Flavell, Richard A

AU - Yao, Yihong

AU - Shen, Nan

PY - 2015/5/12

Y1 - 2015/5/12

N2 - Although different autoimmune diseases show discrete clinical features, there are common molecular pathways intimately involved. Here we show that miR-125a is downregulated in peripheral CD4(+) T cells of human autoimmune diseases including systemic lupus erythematosus and Crohn's disease, and relevant autoimmune mouse models. miR-125a stabilizes both the commitment and immunoregulatory capacity of Treg cells. In miR-125a-deficient mice, the balance appears to shift from immune suppression to inflammation, and results in more severe pathogenesis of colitis and experimental autoimmune encephalomyelitis (EAE). The genome-wide target analysis reveals that miR-125a suppresses several effector T-cell factors including Stat3, Ifng and Il13. Using a chemically synthesized miR-125a analogue, we show potential to re-programme the immune homeostasis in EAE models. These findings point to miR-125a as a critical factor that controls autoimmune diseases by stabilizing Treg-mediated immune homeostasis.

AB - Although different autoimmune diseases show discrete clinical features, there are common molecular pathways intimately involved. Here we show that miR-125a is downregulated in peripheral CD4(+) T cells of human autoimmune diseases including systemic lupus erythematosus and Crohn's disease, and relevant autoimmune mouse models. miR-125a stabilizes both the commitment and immunoregulatory capacity of Treg cells. In miR-125a-deficient mice, the balance appears to shift from immune suppression to inflammation, and results in more severe pathogenesis of colitis and experimental autoimmune encephalomyelitis (EAE). The genome-wide target analysis reveals that miR-125a suppresses several effector T-cell factors including Stat3, Ifng and Il13. Using a chemically synthesized miR-125a analogue, we show potential to re-programme the immune homeostasis in EAE models. These findings point to miR-125a as a critical factor that controls autoimmune diseases by stabilizing Treg-mediated immune homeostasis.

KW - Animals

KW - Case-Control Studies

KW - Colitis

KW - Crohn Disease

KW - Down-Regulation

KW - Homeodomain Proteins

KW - Homeostasis

KW - Humans

KW - Immunity, Cellular

KW - Lupus Erythematosus, Systemic

KW - Mice

KW - Mice, Inbred C57BL

KW - MicroRNAs

KW - Neuritis, Autoimmune, Experimental

KW - T-Lymphocytes, Regulatory

KW - Journal Article

KW - Research Support, Non-U.S. Gov't

U2 - 10.1038/ncomms8096

DO - 10.1038/ncomms8096

M3 - SCORING: Journal article

C2 - 25963922

VL - 6

SP - 7096

JO - NAT COMMUN

JF - NAT COMMUN

SN - 2041-1723

ER -