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Ligation of Na, K ATPase beta 3 subunit on monocytes by a specific monoclonal antibody mediates T cell hypofunction
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Document Title
Ligation of Na, K ATPase beta 3 subunit on monocytes by a specific monoclonal antibody mediates T cell hypofunction
Author
Takheaw N, Laopajon W, Surinkaew S, Khummuang S, Pata S, Kasinrerk W
Name from Authors Collection
Affiliations
Chiang Mai University; Chiang Mai University; National Science & Technology Development Agency - Thailand; National Center Genetic Engineering & Biotechnology (BIOTEC)
Type
Article
Source Title
PLOS ONE
ISSN
1932-6203
Year
2018
Volume
13
Issue
17
Open Access
gold, Green Published, Green Submitted
Publisher
PUBLIC LIBRARY SCIENCE
DOI
10.1371/journal.pone.0199717
Format
Abstract
T cells play a crucial role in orchestrating body immune responses. T cell hyperfunction, however, leads to inflammation and induction of autoimmune diseases. Understanding of T cell regulation mechanisms and successful modulation of T cell responses is beneficial in treatment of disease associated to T cell hyperresponsiveness. Our previous study indicated that monoclonal antibody (mAb) P-3E10, a mAb to Na, K ATPase beta 3 subunit, inhibited anti-CD3-induced PBMC proliferation. In the current study, we further investigated the mechanism of mAb P-3E10 in the induction of T cell hypofunction. We demonstrated that mAb P-3E10 decreased T cell proliferation and Th1, Th2 and Th17 cytokine production. Monocytes were the cells playing a key role in mediation of mAb P-3E10 induced T cell hypofunction. The inhibition of T cell activation by mAb P-3E10 required cell contact between monocytes and T cells. The mAb P-3E10 induced the down-expression level of MHC class II and CD86 and increased IL-6, IL-10 and TNF-alpha production of monocytes. We concluded that ligation of the Na, K ATPase beta 3 subunit on monocytes by mAb P-3E10 arbitrated T cell hypofunction. This mAb might be a promising novel immunotherapeutic antibody for the treatment of hyperresponsive T cell associated diseases.
Funding Sponsor
Thailand Research Fund (TRF) [RTA5980007]; TRF; Thailand Office of Higher Education Commission [MRG6080269]; Royal Golden Jubilee Ph.D. program [PHD/ 0121/2557]; Chiang Mai University
License
CC BY
Rights
Authors
Publication Source
WOS