ArticleInternational journal of nanomedicine2015
Inhibition of myeloid differentiation factor 88 signaling mediated by histidine-grafted poly(β-amino ester) ester nanovector induces donor-specific liver allograft tolerance.
Article in International journal of nanomedicine, 2015. 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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Who cites it
3 citing papers in PubMed, 7 citations in OpenAlex.
- Nanotechnology-Driven Precision Modulation of Transplant Immunity: From Mechanistic Insights to Clinical Tolerance.International journal of nanomedicine · 2026Review
- Engineered Polymeric Nanovector for Intracellular Peptide Delivery in Antitumor Therapy.International journal of nanomedicine · 2023Article
- Polymeric nanomedicines for the treatment of hepatic diseases.Journal of nanobiotechnology · 2022Review
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7 authors at 1 institution in 1 country.
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Abstract
Toll-like receptors (TLRs) activate biochemical pathways that evoke activation of innate immunity, which leads to dendritic cell maturation and initiation of adaptive immune responses that provoke allograft rejection. We aimed to prolong allograft survival by selectively inhibiting expression of myeloid differentiation factor 88 (MyD88), which is an essential adaptor in TLR signaling. We designed and synthesized a novel histidine-grafted poly(β-amino ester) (HGPAE) nanovector, which was shown to be safe and efficient both in vitro and in vivo for the delivery of a plasmid containing shRNA targeting MyD88 (pMyD88). We also demonstrated that the pMyD88/HGPAE complex mediated remarkable inhibition of MyD88 expression in rat liver in vivo. We transplanted Dark Agouti rat livers lacking MyD88 as result of transfection with the pMyD88/HGPAE complex into Lewis rats. The recipients survived longer and graft rejection of the donor liver as well as serum levels of IL-2 and IFN-γ in the recipient were significantly reduced.
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