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P2Y6 Deficiency Enhances Dendritic Cell–Mediated Th1/Th17 Differentiation and Aggravates Experimental Autoimmune Encephalomyelitis

Zhenlong Li, Cong He, Jiang Zhang, Hongmei Zhang, Huan Wei, Shijia Wu and Wenzheng Jiang
J Immunol June 17, 2020, ji1900916; DOI: https://doi.org/10.4049/jimmunol.1900916
Zhenlong Li
Shanghai Key Laboratory of Regulatory Biology, School of Life Sciences, East China Normal University, Shanghai 200241, China
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Cong He
Shanghai Key Laboratory of Regulatory Biology, School of Life Sciences, East China Normal University, Shanghai 200241, China
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Jiang Zhang
Shanghai Key Laboratory of Regulatory Biology, School of Life Sciences, East China Normal University, Shanghai 200241, China
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Hongmei Zhang
Shanghai Key Laboratory of Regulatory Biology, School of Life Sciences, East China Normal University, Shanghai 200241, China
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Huan Wei
Shanghai Key Laboratory of Regulatory Biology, School of Life Sciences, East China Normal University, Shanghai 200241, China
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Shijia Wu
Shanghai Key Laboratory of Regulatory Biology, School of Life Sciences, East China Normal University, Shanghai 200241, China
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Wenzheng Jiang
Shanghai Key Laboratory of Regulatory Biology, School of Life Sciences, East China Normal University, Shanghai 200241, China
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Key Points

  • P2Y6 deficiency enhances DC-mediated Th1/Th17 differentiation.

  • P2Y6 deficiency aggravates the pathogenesis of EAE.

Abstract

Dendritic cells (DCs) are essential APCs and play a crucial role in initiating and regulating the adaptive immune response. In this study, we have reported that P2Y6, a member of G protein–coupled receptors, inhibits the maturation and activation of DCs via suppressing the activation of the transcription factor NF-κB. Furthermore, loss of P2Y6 does not impact T cells homeostasis in the steady-state. However, in vitro studies show that P2Y6 signaling inhibits the production of IL-12 and IL-23 and the polarization of Th1 and Th17 subsets mediated by DCs. In addition, we find that mice lacking P2Y6 develop more severe experimental autoimmune encephalomyelitis compared with wild-type mice. Our results indicate that P2Y6 functions as a pivotal regulator on DC maturation, and the loss of P2Y6 results in the aggravated experimental autoimmune encephalomyelitis, which suggests that P2Y6 may play a pivotal role in the pathogenesis of autoimmune diseases.

Footnotes

  • This work was supported by the National Natural Science Foundation of China (81771306, 81072459), the National Key Research and Development Program of China (2016YFC1200400), the Program for New Century Excellent Talents in University (NCET-12-0179), and the Science and Technology Commission of Shanghai Municipality (14140904200).

  • The online version of this article contains supplemental material.

  • Received August 1, 2019.
  • Accepted May 14, 2020.
  • Copyright © 2020 by The American Association of Immunologists, Inc.

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The Journal of Immunology: 206 (5)
The Journal of Immunology
Vol. 206, Issue 5
1 Mar 2021
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P2Y6 Deficiency Enhances Dendritic Cell–Mediated Th1/Th17 Differentiation and Aggravates Experimental Autoimmune Encephalomyelitis
Zhenlong Li, Cong He, Jiang Zhang, Hongmei Zhang, Huan Wei, Shijia Wu, Wenzheng Jiang
The Journal of Immunology June 17, 2020, ji1900916; DOI: 10.4049/jimmunol.1900916

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P2Y6 Deficiency Enhances Dendritic Cell–Mediated Th1/Th17 Differentiation and Aggravates Experimental Autoimmune Encephalomyelitis
Zhenlong Li, Cong He, Jiang Zhang, Hongmei Zhang, Huan Wei, Shijia Wu, Wenzheng Jiang
The Journal of Immunology June 17, 2020, ji1900916; DOI: 10.4049/jimmunol.1900916
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Print ISSN 0022-1767        Online ISSN 1550-6606