Figure - PMC

Skip to main content

An official website of the United States government

Here's how you know

Here's how you know

Official websites use .gov
A .gov website belongs to an official government organization in the United States.

Secure .gov websites use HTTPS
A lock ( ) or https:// means you've safely connected to the .gov website. Share sensitive information only on official, secure websites.

View full-text article in PMC

. 2020 Jul 22;11:304. doi: 10.1186/s13287-020-01799-0

Search in PMC
Search in PubMed
View in NLM Catalog
Add to search

© The Author(s) 2020

Open AccessThis article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated in a credit line to the data.

PMC Copyright notice

Fig. 3 — Canine ASCs and PMSCs inhibit lymphocyte proliferation in a contact-dependent manner. Canine adipose-derived MSCs (ASCs) and placenta-derived MSCs (PMSCs) possess immune-suppressive functions. a Canine ASCs and PMSCs co-incubated with stimulated peripheral blood mononuclear cells (PBMCs) suppress lymphocyte proliferation. PMSCs significantly decrease lymphocyte proliferation more potently as compared to ASCs. Transwells were added to remove physical contact between MSCs and mitogen (ConA) stimulated PBMCs. Lymphocyte proliferation increased when ASCs and PMSCs were not in direct contact with activated PBMCs. b To determine the role of indoleamine 2,3 dioxygenase (IDO) and prostaglandin E₂ (PGE₂) in MSC-mediated immunosuppression 1-methyl-DL-tryptophan (1-MT) and indomethacin was added to co-cultures to block each respective mediator. Blocking of IDO activity using 1-MT resulted in no alterations in MSC-mediated suppression of PBMC proliferation. Blocking PGE₂ using indomethacin resulted in a loss of lymphocyte inhibition by ASCs but no effects were observed by PMSCs. PBMC stimulation is normalized and data is presented as a reduction to each respective donor. Representative photomicrographs of ConA stimulated PBMCs and PMSC LSA conditions (c). Data presented as mean and standard error. *p < 0.05, **p < 0.01, ***p < 0.001. 1-MT, 1-methyl-DL-tryptophan; ConA, concanavalin A; IDO, indoleamine 2,3 dioxygenase; LSA, leukocyte suppression assay; MSC, mesenchymal stem cell; PBMCs, peripheral blood mononuclear cells; PGE₂, prostaglandin E₂