Asset Details
Do you wish to reserve the book?
Mesenchymal Stem Cells Repress Th17 Molecular Program through the PD-1 Pathway
Hey, we have placed the reservation for you!
By the way, why not check out events that you can attend while you pick your title.
Oops! Something went wrong.
Looks like we were not able to place the reservation. Kindly try again later.
Are you sure you want to remove the book from the shelf?
Mesenchymal Stem Cells Repress Th17 Molecular Program through the PD-1 Pathway
Do you wish to request the book?
Mesenchymal Stem Cells Repress Th17 Molecular Program through the PD-1 Pathway
Please be aware that the book you have requested cannot be checked out. If you would like to checkout this book, you can reserve another copy
We have requested the book for you!
Your request is successful and it will be processed during the Library working hours. Please check the status of your request in My Requests.
Oops! Something went wrong.
Looks like we were not able to place your request. Kindly try again later.
Journal Article
Mesenchymal Stem Cells Repress Th17 Molecular Program through the PD-1 Pathway
2012
Overview
MSC display potent suppressive properties initially described a decade ago. More recently, MSC suppressive activities on T-cell effector pathways have been investigated. MSC modulate CD4 differentiation through different mechanisms depending on culture conditions and display disparate activities on T cells according to their differentiation status. A significant amount of evidence for MSC effects on Th17 cells revealed that MSC could be suppressive under diverse circumstances but also enhance Th17 cell activity under other conditions. In the present study, we investigated the suppressive effects of MSC on Th1 and Th17 subsets of T cells using T cells undergoing Th1 and Th17 polarization or mature Th1 and Th17 cells. MSC inhibited the proliferation of T cells during their differentiation toward Th1 cells and mature Th1 cells. This suppressive effect was maintained in a transwell cell culture insert demonstrating the major role played by soluble factors. Using the transwell cell separation barrier, we observed that MSC decrease the number of T cells undergoing Th17 differentiation whereas they did not affect IL-17 production by mature Th17, demonstrating the need for cell contact for suppressing Th17 cell function. Moreover, we reported that PD-L1 is highly expressed on MSC co-cultured with differentiating or polarized Th1 and Th17 cells. Using neutralizing antibodies specific for PD-L1 and PD-1 we showed that the mechanisms by which MSC mediate Th17 cell repolarization depend on PD-L1 expression on MSC. Taken together our results demonstrated a cell-to-cell contact depend mechanism in the selective immunosuppression of MSC on mature Th17 cells through up-regulation of PD-L1.
Publisher
Public Library of Science,Public Library of Science (PLoS)
Subject
/ Antibodies, Neutralizing - pharmacology
/ Antigens
/ B7-H1 Antigen - antagonists & inhibitors
/ Biology
/ Cell Communication - genetics
/ Cell Differentiation - drug effects
/ Cell Proliferation - drug effects
/ Gene Expression Regulation - drug effects
/ Interleukin-17 - biosynthesis
/ Mesenchymal Stromal Cells - cytology
/ Mesenchymal Stromal Cells - metabolism
/ Mice
/ Programmed Cell Death 1 Receptor - antagonists & inhibitors
/ Programmed Cell Death 1 Receptor - genetics
/ Programmed Cell Death 1 Receptor - metabolism
/ Rodents
/ Signal Transduction - drug effects
/ Signal Transduction - genetics
/ Studies
/ T cells
