Combined liver–cytokine humanization comes to the rescue of circulating human red blood cells | Zendy

Yuanbin Song | Zendy; Liang Shan | Zendy; Rana Gbyli | Zendy; Wei Liu | Zendy; Till Strowig | Zendy; Amisha Patel | Zendy; Xiaoying Fu | Zendy; Xiaman Wang | Zendy; Mina L. Xu | Zendy; Yimeng Gao | Zendy; Ashley Qin | Zendy; Emanuela M. Bruscia | Zendy; Toma Tebaldi | Zendy; Giulia Biancon | Zendy; Padmavathi Mamillapalli | Zendy; David Urbonas | Zendy; Elizabeth E. Ey | Zendy; David G. Gonzalez | Zendy; Jie Chen | Zendy; Diane S. Krause | Zendy; Jonathan Alderman | Zendy; Stephanie Halene | Zendy; Richard A. Flavell | Zendy

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Combined liver–cytokine humanization comes to the rescue of circulating human red blood cells

Author(s) -

Yuanbin Song,

Liang Shan,

Rana Gbyli,

Wei Liu,

Till Strowig,

Amisha Patel,

Xiaoying Fu,

Xiaman Wang,

Mina L. Xu,

Yimeng Gao,

Ashley Qin,

Emanuela M. Bruscia,

Toma Tebaldi,

Giulia Biancon,

Padmavathi Mamillapalli,

David Urbonas,

Elizabeth E. Ey,

David G. Gonzalez,

Jie Chen,

Diane S. Krause,

Jonathan Alderman,

Stephanie Halene,

Richard A. Flavell

Publication year - 2021

Publication title -

science

Language(s) - English

Resource type - Journals

SCImago Journal Rank - 12.556

H-Index - 1186

eISSN - 1095-9203

pISSN - 0036-8075

DOI - 10.1126/science.abe2485

Subject(s) - erythropoiesis , haematopoiesis , biology , immunology , red blood cell , liver disease , fetus , cytokine , stem cell , microbiology and biotechnology , anemia , medicine , genetics , pregnancy , biochemistry

A red-letter day for RBC research The study of primary human red blood cell (huRBC) disorders such as sickle cell disease (SCD) and infectious diseases such as malaria has been hampered by a lack of in vivo models of human erythropoiesis. Songet al. transferred human fetal liver cells into MISTRG mice, which are immunodeficient and are genetically engineered with several human genes involved in hematopoiesis. This approach was unsuccessful because mature huRBCs are rapidly destroyed in the mouse liver. They then used CRISPR-Cas9 to mutate these mice into a fumarylacetoacetate hydrolase–deficient strain, allowing them to replace the mouse liver with engrafted human hepatocytes. These mice exhibited enhanced human erythropoiesis and circulating huRBC survival and could recapitulate SCD pathology when reconstituted with SCD-derived HSCs.Science , this issue p.1019

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