Literature DB >> 23994719

The suppression of inflammatory macrophage-mediated cytotoxicity and proinflammatory cytokine production by transgenic expression of HLA-E.

Akira Maeda1, Takuji Kawamura, Takehisa Ueno, Noriaki Usui, Hiroshi Eguchi, Shuji Miyagawa.   

Abstract

BACKGROUND: Macrophages participate in xenogenic rejection and represent a major biological obstacle to successful xenotransplantation. The signal inhibitory regulatory protein α (SIRPα) receptor was reported to be a negative regulator of macrophage phagocytic activity via interaction with CD47, its ligand. Because a majority of human macrophages express the inhibitory receptor CD94/NKG2A, which binds specifically to the human leukocyte antigen (HLA)-E and contains immunoreceptor tyrosine-based inhibition motifs (ITIMs), the inhibitory function of HLA class I molecules, HLA-E, on macrophage-mediated cytolysis was examined. The suppressive effect against proinflammatory cytokine production by macrophages was also examined.
METHODS: Complementary DNA (cDNA) of HLA-E, and CD47 were prepared and transfected into swine endothelial cells (SEC). The expression of the modified genes was evaluated by flow cytometry and macrophage-mediated cytolysis was assessed using in vitro generated macrophages.
RESULTS: Transgenic expression of HLA-E significantly suppressed the macrophage-mediated cytotoxicity. HLA-E transgenic expression demonstrated a significant suppression equivalent to CD47 transgenic expression. Furthermore, transgenic HLA-E suppressed the production of pro-inflammatory cytokines by inflammatory macrophages.
CONCLUSIONS: These results indicate that generating transgenic HLA-E pigs might protect porcine grafts from, not only NK cytotoxicity, but also macrophage-mediated cytotoxicity.
© 2013 Elsevier B.V. All rights reserved.

Entities:  

Keywords:  HLA-E; Immunoreceptor tyrosine-based inhibition motif (ITIM); Inflammatory macrophage; Pro-inflammatory cytokine; Xenocytotoxicity

Mesh:

Substances:

Year:  2013        PMID: 23994719     DOI: 10.1016/j.trim.2013.08.001

Source DB:  PubMed          Journal:  Transpl Immunol        ISSN: 0966-3274            Impact factor:   1.708


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