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Abstract/Summary
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<jats:p>Despite recent advances in immunodeficient mouse models bearing human red blood cells (hRBCs), the elimination of circulating hRBCs by residual innate immune systems remains a significant challenge. In this study, we evaluated the role of mouse complement C3 in the elimination of circulating hRBCs by developing a novel NOG substrain harboring a truncated version of the murine C3 gene (NOG-C3<jats:sup>ΔMG2-3</jats:sup>). Genetic C3 deletion prolonged the survival of transfused hRBCs in the circulation. Chemical depletion and functional impairment of mouse macrophages, using clodronate liposomes (Clo-lip) or gadolinium chloride (GdCl<jats:sub>3</jats:sub>), respectively, further extended the survival of hRBCs in NOG-C3<jats:sup>ΔMG2-3</jats:sup> mice. Low GdCl<jats:sub>3</jats:sub> toxicity allowed the establishment of hRBC-bearing mice, in which hRBCs survived for more than 4 weeks with transfusion once a week. In addition, erythropoiesis of human hematopoietic stem cells (hHSCs) was possible in NOG-C3<jats:sup>ΔMG2-3</jats:sup>/human GM-CSF-IL-3 transgenic mice with Clo-lip treatment. These findings indicate that mouse models harboring hRBCs can be achieved using NOG-C3<jats:sup>ΔMG2-3</jats:sup> mice, which could facilitate studies of human diseases associated with RBCs.</jats:p>
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1000
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Hinweis
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DeepGreen-ID: 9c0b0b4582194412b7e8a57f193642b2 ; metadata provieded by: DeepGreen (https://www.oa-deepgreen.de/api/v1/), LIVIVO search scope life sciences (http://z3950.zbmed.de:6210/livivo), Crossref Unified Resource API (https://api.crossref.org/swagger-ui/index.html), to.science.api (https://frl.publisso.de/), ZDB JSON-API (beta) (https://zeitschriftendatenbank.de/api/), lobid - Dateninfrastruktur für Bibliotheken (https://lobid.org/resources/search)
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