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However, the therapeutic mechanism is not clear. The present study was undertaken to investigate whether ecto-5\u2032-nucleotidase (CD73) expression on ERCs is critical to cardiac allograft protection. C57BL\/6 mouse recipients receiving BALB\/c mouse cardiac allografts were treated with unmodified ERCs or anti-CD73 monoclonal antibodies (mAb) pretreated ERCs, respectively. It has been found that CD73 expression was critical to ERC-induced attenuation of graft pathology. The blockage of CD73 expression on ERCs was related to the percentage decline of tolerogenic dendritic cells (Tol-DCs), macrophages type 2 (M2), and regulatory T cells (Tregs). As compared with anti-CD73 mAb pretreated ERCs group, CD73 expressing ERCs significantly increased the level of anti-inflammatory cytokine IL-10 but decreased levels of pro-inflammatory cytokines including IFN-\u03b3 and TNF-\u03b1. In addition, CD73 expressing ERCs showed tissue protective function via the regulation of adenosine receptor expression which was related to the infiltration of CD4+ and CD8+ cells in the allografts. Furthermore, significant increase of A2B receptors in the cardiac allograft was also associated with CD73 expressing ERC-induced prolongation of cardiac allograft survival.<\/jats:p>","DOI":"10.1002\/sctm.20-0154","type":"journal-article","created":{"date-parts":[[2020,10,30]],"date-time":"2020-10-30T10:24:22Z","timestamp":1604053462000},"page":"465-478","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":13,"title":["CD73 expression is critical to therapeutic effects of human endometrial regenerative cells in inhibition of cardiac allograft rejection in mice"],"prefix":"10.1093","volume":"10","author":[{"given":"Yonghao","family":"Hu","sequence":"first","affiliation":[{"name":"Department of General Surgery Tianjin Medical University General Hospital, Tianjin, People's Republic of China"},{"name":"Tianjin General Surgery Institute, Tianjin, People's Republic of 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