Human reconstituting hematopoietic stem cells up-regulate Fas expression upon active cell cycling but remain resistant to Fas-induced suppression.

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Dybedal, Ingunn (author)

Human reconstituting hematopoietic stem cells up-regulate Fas expression upon active cell cycling but remain resistant to Fas-induced suppression.

Article/chapterEnglish2003

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American Society of Hematology,2003

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LIBRIS-ID:oai:lup.lub.lu.se:bbc2326e-1734-4073-92e1-cc7a60f3d7aa
https://lup.lub.lu.se/record/112804URI
https://doi.org/10.1182/blood-2002-07-2286DOI

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Language:English
Summary in:English

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The Fas receptor and its ligand have been implicated in mediating the bone marrow (BM) suppression observed in graft-versus-host disease and a number of other BM-failure syndromes. However, previous studies have suggested that Fas is probably not expressed on human hematopoietic stem cells (HSCs), but up-regulated as a consequence of their commitment and differentiation, suggesting that progenitors or differentiated blood cells, rather than HSCs, are the targets of Fas-mediated suppression. The present studies confirm that candidate HSCs in human cord blood and BM lack constitutive expression of Fas, but demonstrate that Fas expression on CD34+ progenitor and stem cells is correlated to their cell cycle and activation status. With the use of recently developed in vitro conditions promoting HSC self-renewing divisions, Fas was up-regulated on virtually all HSCs capable of multilineage reconstituting nonobese diabetic/severe combined immunodeficiency (NOD-SCID) mice in vivo, as well as on long-term culture-initiating cells (LTC-ICs). Similarly, in vivo cycling of NOD-SCID repopulating cells upon transplantation, resulted in up-regulation of Fas expression. However, repopulating HSCs expressing high levels of Fas remained highly resistant to Fas-mediated suppression, and HSC function was compromised only upon coactivation with tumor necrosis factor. Thus, reconstituting human HSCs up-regulate Fas expression upon active cycling, demonstrating that HSCs could be targets for Fas-mediated BM suppression. (Blood. 2003;102: 118-126)

Subject headings and genre

MEDICIN OCH HÄLSOVETENSKAP Klinisk medicin Hematologi hsv//swe
MEDICAL AND HEALTH SCIENCES Clinical Medicine Hematology hsv//eng

Added entries (persons, corporate bodies, meetings, titles ...)

Yang, LipingLund University,Lunds universitet,Stamcellscentrum (SCC),Avdelningen för stamcellsforskning,Institutionen för laboratoriemedicin,Medicinska fakulteten,Stem Cell Center,Division of stem cell research,Department of Laboratory Medicine,Faculty of Medicine(Swepub:lu)stam-lya (author)
Bryder, DavidLund University,Lunds universitet,Institutionen för laboratoriemedicin,Medicinska fakulteten,Department of Laboratory Medicine,Faculty of Medicine(Swepub:lu)med-dbr (author)
Åstrand-Grundström, IngbrittLund University,Lunds universitet,Stamcellscentrum (SCC),Avdelningen för stamcellsforskning,Institutionen för laboratoriemedicin,Medicinska fakulteten,Stem Cell Center,Division of stem cell research,Department of Laboratory Medicine,Faculty of Medicine(Swepub:lu)molm-iag (author)
Leandersson, KarinLund University,Lunds universitet,Cancerimmunologi, Malmö,Forskargrupper vid Lunds universitet,Cancer Immunology, Malmö,Lund University Research Groups(Swepub:lu)immu-kpe (author)
Jacobsen, Sten Eirik WLund University,Lunds universitet,Stamcellscentrum (SCC),Avdelningen för stamcellsforskning,Institutionen för laboratoriemedicin,Medicinska fakulteten,Stem Cell Center,Division of stem cell research,Department of Laboratory Medicine,Faculty of Medicine(Swepub:lu)stem-sja (author)
Stamcellscentrum (SCC)Avdelningen för stamcellsforskning (creator_code:org_t)

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In:Blood: American Society of Hematology102:1, s. 118-1261528-00200006-4971

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By the author/editor: Dybedal, Ingunn; Yang, Liping; Bryder, David; Åstrand-Grundstr ...; Leandersson, Kar ...; Jacobsen, Sten E ...

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