About: A New Immunosuppressive Molecule Emodin Induces both CD4(+)FoxP3(+) and CD8(+)CD122(+) Regulatory T Cells and Suppresses Murine Allograft Rejection

Facets (new session)
Description
Metadata
Settings
- owl:sameAs
- Inference Rule:

About: A New Immunosuppressive Molecule Emodin Induces both CD4(+)FoxP3(+) and CD8(+)CD122(+) Regulatory T Cells and Suppresses Murine Allograft Rejection Goto Sponge NotDistinct Permalink

An Entity of Type : schema:ScholarlyArticle, within Data Space : wasabi.inria.fr associated with source document(s)

Attributes	Values
type	Academic Article research paper schema:ScholarlyArticle
isDefinedBy	Covid-on-the-Web dataset
has title	A New Immunosuppressive Molecule Emodin Induces both CD4(+)FoxP3(+) and CD8(+)CD122(+) Regulatory T Cells and Suppresses Murine Allograft Rejection
Creator	Dai, Zhenhua Liang, Chun-Ling Liu, Huazhen Qiu, Feifei Nie, Golay Zhang, Lal, Girdhari Zheng, Jenny
Source	Medline; PMC
abstract	Due to vigorous alloimmunity, an allograft is usually rejected without any conventional immunosuppressive treatment. However, continuous global immunosuppression may cause severe side effects, including tumors and infections. Mounting evidence has shown that cyclosporine (CsA), a common immunosuppressant used in clinic, impedes allograft tolerance by dampening regulatory T cells (Tregs), although it inhibits allograft rejection at the same time. Therefore, it is necessary to seek an alternative immunosuppressive drug that spares Tregs with high efficiency in suppression but low toxicity. In this study, we investigated the capacity of emodin, an anthraquinone molecule originally extracted from certain natural plants, to prolong transplant survival in a mouse model and explored the cellular and molecular mechanisms underlying its action. We found that emodin significantly extended skin allograft survival and hindered CD3(+) T cell infiltration in the allograft, accompanied by an increase in CD4(+)Foxp3(+) and CD8(+)CD122(+) Treg frequencies and numbers but a reduction in effector CD8(+)CD44(high)CD62L(low) T cells in recipient mice. Emodin also inhibited effector CD8(+) T cells proliferation in vivo. However, CD4(+)CD25(+), but not CD8(+)CD122(+), Tregs derived from emodin-treated recipients were more potent in suppression of allograft rejection than those isolated from control recipients, suggesting that emodin also enhances the suppressive function of CD4(+)CD25(+) Tregs. Interestingly, depleting CD25(+) Tregs largely reversed skin allograft survival prolonged by emodin while depleting CD122(+) Tregs only partially abrogated the same allograft survival. Furthermore, we found that emodin hindered dendritic cell (DC) maturation and reduced alloantibody production posttransplantation. Finally, we demonstrated that emodin inhibited in vitro proliferation of T cells and blocked their mTOR signaling as well. Therefore, emodin may be a novel mTOR inhibitor that suppresses alloimmunity by inducing both CD4(+)FoxP3(+) and CD8(+)CD122(+) Tregs, suppressing alloantibody production, and hindering DC maturation. Thus, emodin is a newly emerging immunosuppressant and could be utilized in clinical transplantation in the future.
has issue date	2017-11-08(xsd:dateTime)
bibo:doi	10.3389/fimmu.2017.01519
bibo:pmid	29167674
has license	cc-by
sha1sum (hex)	04bc03c90437934a75fc6fdc228817234ef84c3a
schema:url	https://doi.org/10.3389/fimmu.2017.01519
resource representing a document's title	A New Immunosuppressive Molecule Emodin Induces both CD4(+)FoxP3(+) and CD8(+)CD122(+) Regulatory T Cells and Suppresses Murine Allograft Rejection
has PubMed Central identifier	PMC5682309
has PubMed identifier	29167674
schema:publication	Front Immunol
resource representing a document's body	covid:04bc03c90437934a75fc6fdc228817234ef84c3a#body_text
is schema:about of	named entity 'MOLECULE' named entity 'REGULATORY T CELLS' named entity 'TRANSPLANTED' named entity 'MEANS' named entity 'NUMBERS' named entity 'SEPARATE' named entity 'CSA' named entity 'LNS' named entity 'ABSOLUTE' named entity 'EMODIN' named entity 'FLOW CYTOMETER' named entity 'MICE' named entity 'NEW' named entity 'CD4' named entity 'IMMUNOSUPPRESSIVE' named entity 'REGULATORY T CELLS' named entity 'ALLOGRAFT REJECTION' named entity 'CD8' named entity 'SUPPRESSES' named entity 'ONE OF' named entity 'ISOLATED' named entity 'CELLS' named entity 'EMODIN' named entity 'CD8' named entity 'SKIN' named entity 'DRAINING LYMPH NODE' named entity 'FIGURE' named entity 'MURINE' named entity 'SPLEEN' named entity 'MEASURED' named entity 'CD122' named entity 'CD122' named entity 'DAYS' named entity 'EXPERIMENTS' named entity 'TRANSPLANTATION' named entity 'BALB' named entity 'DATA' named entity 'TREATED' named entity 'FOXP3' named entity 'RECIPIENT' named entity 'CD122' named entity 'CD8 +' named entity 'spleens' named entity 'CD122' named entity 'CsA' named entity 'mice' named entity 'Murine' named entity 'emodin' named entity 'allograft' named entity 'allograft' named entity 'toxicity' named entity 'alloantibody' named entity 'allotransplantation' named entity 'mTOR' named entity 'CD122' named entity 'skin graft' named entity 'Foxp3' named entity 'allograft' named entity 'cD4 +' named entity 'mTOR' named entity 'mTOR' named entity 'emodin' named entity 'allograft' named entity 'phosphorylation' named entity 'Treg' named entity 'western blotting' named entity 'mTOR inhibitor' named entity 'spleens' named entity 'cell apoptosis' named entity 'sodium' named entity 'Tregs' named entity 'cyclosporine' named entity 'emodin' named entity 'FoxP3'

Faceted Search & Find service v1.13.91 as of Mar 24 2020

Alternative Linked Data Documents: Sponger | ODE Content Formats:

RDF

ODATA

Microdata

About

OpenLink Virtuoso version 07.20.3229 as of Jul 10 2020, on Linux (x86_64-pc-linux-gnu), Single-Server Edition (94 GB total memory)
Data on this page belongs to its respective rights holders.
Virtuoso Faceted Browser Copyright © 2009-2024 OpenLink Software