Cited by 484Phagocytosis and Immune RegulationIron Metabolism and DisordersImmune cells in cancer

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Role for Spi-C in the development of red pulp macrophages and splenic iron homeostasis

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Kohyama, Masako, Ise, Wataru, Edelson, Brian T., Wilker, Peter R., Hildner, Kai, Mejia, Carlo, Frazier, William A., Murphy, Theresa L., Murphy, Kenneth M.·2009·Nature

DOI 10.1038/nature07472PMC PMC2756102

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Abstract

Tissue macrophages comprise a heterogeneous group of cell types differing in location, surface markers and function. Red pulp macrophages are a distinct splenic subset involved in removing senescent red blood cells. Transcription factors such as PU.1 (also known as Sfpi1) and C/EBPalpha (Cebpa) have general roles in myelomonocytic development, but the transcriptional basis for producing tissue macrophage subsets remains unknown. Here we show that Spi-C (encoded by Spic), a PU.1-related transcription factor, selectively controls the development of red pulp macrophages. Spi-C is highly expressed in red pulp macrophages, but not monocytes, dendritic cells or other tissue macrophages. Spic(-/-) mice have a cell-autonomous defect in the development of red pulp macrophages that is corrected by retroviral Spi-C expression in bone marrow cells, but have normal monocyte and other macrophage subsets. Red pulp macrophages highly express genes involved in capturing circulating haemoglobin and in iron regulation. Spic(-/-) mice show normal trapping of red blood cells in the spleen, but fail to phagocytose these red blood cells efficiently, and develop an iron overload localized selectively to splenic red pulp. Thus, Spi-C controls development of red pulp macrophages required for red blood cell recycling and iron homeostasis.

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Authors: Kohyama, M., Ise, W., Edelson, B. T., Wilker, P. R., Hildner, K., Mejia, C., Frazier, W. A., Murphy, T. L., & Murphy, K. M.
Affiliations: Washington University in St. Louis (US)
Howard Hughes Medical Institute (US)
Corresponding author: Murphy, Kenneth M.
ORCID: Ise, Wataru
Edelson, Brian T.
Hildner, Kai
Murphy, Kenneth M.
Venue: Nature
Publisher: Springer Science and Business Media LLC
Published: 2008-11-26
Volume: 457
Issue: 7227
Pages: 318-321
ISSN: 0028-0836 (ISSN-L)
1476-4687
DOI: 10.1038/nature07472
PMC: PMC2756102
OpenAlex: W2065338876
Cited by: 479
References: 30
Citations by year: 2026: 36 · 2025: 28 · 2024: 30 · 2023: 23 · 2022: 47 · 2021: 45 · 2020: 41 · 2019: 22 · 2018: 35 · 2017: 29 · 2016: 36 · 2015: 36 · 2014: 22 · 2013: 20 · 2012: 18
FWCI: 1.40
Type: journal article
Language: en
Open access: green
www.ncbi.nlm.nih.gov
Licence: www.springer.com/tdm (tdm)
Locations: Nature (publishedVersion)
PubMed (publishedVersion)
Europe PMC (PubMed Central) (acceptedVersion)
PubMed Central (acceptedVersion)
RePEc: Research Papers in Economics (submittedVersion)
Funders: Howard Hughes Medical Institute
Topics: Life Sciences › Immunology and Microbiology › Immunology › Phagocytosis and Immune Regulation
Health Sciences › Medicine › Hematology › Iron Metabolism and Disorders
Life Sciences › Immunology and Microbiology › Immunology › Immune cells in cancer
Keywords: SPIC, red pulp macrophages, spleen, iron homeostasis, iron overload, erythrophagocytosis, senescent red blood cells, transcription factors
MeSH terms: Animals, Cell Count, DNA-Binding Proteins, Erythrocytes, Gene Expression Regulation, Homeostasis, Iron, Macrophages, Phagocytosis, Spleen, Vascular Cell Adhesion Molecule-1, Mice

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Role for Spi-C in the development of red pulp macrophages and splenic iron homeostasis

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