ArticleFASEB bioAdvances2019
ECDI-fixed donor splenocytes prolong skin allograft survival by promoting M2 macrophage polarization and inducing regulatory T cells.
Article in FASEB bioAdvances, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
3 citing papers in PubMed, 5 citations in OpenAlex.
- The role of macrophage polarization in organ transplantation: research progress on impact on graft injury, repair, and fibrosis.Frontiers in immunology · 2026Review
- M2 macrophage polarization in allogeneic skin transplantation: from intrinsic mechanisms to clinical prospects for immune tolerance.Molecular biology reports · 2025Review
- ECDI-fixed donor splenocytes prolong skin allograft survival by promoting M2 macrophage polarization and inducing regulatory T cells.FASEB bioAdvances · 2019Article
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Authors and funding
10 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Rejection is a common complication of allogeneic tissue transplantation. Fixation of splenocytes (SP) with 1-ethyl-3-(3'-dimethylaminopropyl)-carbodiimide (ECDI) induces immune tolerance in recipients post-transplantation; however, the mechanism underlying this effect remains unclear. Here, we determined the mechanisms of ECDI-fixed donor SP (ECDI-SP) in inducing tolerance in skin allograft transplantation. C57BL/6-recipient mice that received Balb/c full-thickness skin transplants with two infusions of donor-derived ECDI-SP, along with rapamycin showed superior skin allograft survival and lower inflammatory cell infiltration than mice that received rapamycin-only treatment. In ECDI-SP-treated mice, the levels of anti-inflammatory cytokines such as interleukin (IL)-10 in sera were markedly increased, whereas the expression of inflammatory cytokines was significantly suppressed. Splenic macrophages were significantly polarized to the alternative activated macrophage (M2) phenotype, with expansion of CD4
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