Human CD200 suppresses macrophage-mediated xenogeneic cytotoxicity and phagocytosis View Full Text


Ontology type: schema:ScholarlyArticle     


Article Info

DATE

2017-06-01

AUTHORS

Rieko Sakai, Akira Maeda, Thuy-Vy Choi, Pei-Chi Lo, Patmika Jiaravuthisan, Afifah Mod Shabri, Han-Tang Wang, Rei Matsuura, Tasuku Kodama, Hiroshi Eguchi, Hiroomi Okuyama, Shuji Miyagawa

ABSTRACT

PurposeVarious strategies, such as the generation of alpha-1,3-galactosyltransferase knocked-out pigs and CD55 transgenic pigs, have been investigated to inhibit pig to human xenogeneic rejection. Our aim is to develop strategies to overcome the hurdle of not only hyper acute rejection, but also that of cellular xenogeneic rejection (CXR). Although macrophages have been well known to play a critical role in CXR, monocyte/macrophage-mediated xenogeneic rejection has not been well studied. In this study, we evaluated the effect of CD200 in xenogeneic rejection by macrophages.MethodsNaïve swine endothelial cells (SEC) and SEC/CD200 were co-cultured with M0 macrophages and the cytotoxicity was measured by a WST-8 assay. The phagocytosis of SEC and SEC/CD200 by macrophages was analyzed by flow cytometry.ResultsWhile CD200 failed to suppress a significant amount of cytotoxicity against SEC by monocytes, M0 macrophage-mediated cytotoxicity was significantly suppressed by human CD200. The phagocytosis by M0 macrophages was also tested. The phagocytosis assay revealed that human CD200 suppresses M0 macrophage-mediated phagocytosis.ConclusionsOur findings indicate that human CD200 suppresses the xenogeneic rejection by CD200R+ macrophages and that the generation of hCD200 transgenic pigs for use in xenografts is very attractive for preventing the macrophage-mediated rejection. More... »

PAGES

119-126

References to SciGraph publications

Identifiers

URI

http://scigraph.springernature.com/pub.10.1007/s00595-017-1546-2

DOI

http://dx.doi.org/10.1007/s00595-017-1546-2

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1085738166

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/28573328


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