Journal
JOURNAL OF IMMUNOLOGY
Volume 205, Issue 2, Pages 387-397Publisher
AMER ASSOC IMMUNOLOGISTS
DOI: 10.4049/jimmunol.1900916
Keywords
-
Categories
Funding
- National Natural Science Foundation of China [81771306, 81072459]
- National Key Research and Development Program of China [2016YFC1200400]
- Program for New Century Excellent Talents in University [NCET-12-0179]
- Science and Technology Commission of Shanghai Municipality [14140904200]
Ask authors/readers for more resources
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 P2Y(6), a member of G protein-coupled receptors, inhibits the maturation and activation of DCs via suppressing the activation of the transcription factor NF-kappa B. Furthermore, loss of P2Y(6) does not impact T cells homeostasis in the steady-state. However, in vitro studies show that P2Y(6) 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 P2Y 6 develop more severe experimental autoimmune encephalomyelitis compared with wild-type mice. Our results indicate that P2Y(6) functions as a pivotal regulator on DC maturation, and the loss of P2Y(6) results in the aggravated experimental autoimmune encephalomyelitis, which suggests that P2Y(6) may play a pivotal role in the pathogenesis of autoimmune diseases.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available