Format

Send to

Choose Destination
See comment in PubMed Commons below
Blood. 2012 Jul 5;120(1):76-85. doi: 10.1182/blood-2011-12-399113. Epub 2012 May 18.

Critical role of P1-Runx1 in mouse basophil development.

Author information

1
Department of Pathology, Stanford University School of Medicine, Stanford, CA 94305, USA.

Abstract

Runx1(P1N/P1N) mice are deficient in the transcription factor distal promoter-derived Runt-related transcription factor 1 (P1-Runx1) and have a > 90% reduction in the numbers of basophils in the BM, spleen, and blood. In contrast, Runx1(P1N/P1N) mice have normal numbers of the other granulocytes (neutrophils and eosinophils). Although basophils and mast cells share some common features, Runx1(P1N/P1N) mice have normal numbers of mast cells in multiple tissues. Runx1(P1N/P1N) mice fail to develop a basophil-dependent reaction, IgE-mediated chronic allergic inflammation of the skin, but respond normally when tested for IgE- and mast cell-dependent passive cutaneous anaphylaxis in vivo or IgE-dependent mast cell degranulation in vitro. These results demonstrate that Runx1(P1N/P1N) mice exhibit markedly impaired function of basophils, but not mast cells. Infection with the parasite Strongyloides venezuelensis and injections of IL-3, each of which induces marked basophilia in wild-type mice, also induce modest expansions of the very small populations of basophils in Runx1(P1N/P1N) mice. Finally, Runx1(P1N/P1N) mice have normal numbers of the granulocyte progenitor cells, SN-Flk2(+/-), which can give rise to all granulocytes, but exhibit a > 95% reduction in basophil progenitors. The results of the present study suggest that P1-Runx1 is critical for a stage of basophil development between SN-Flk2(+/-) cells and basophil progenitors.

PMID:
22611151
PMCID:
PMC3390962
DOI:
10.1182/blood-2011-12-399113
[Indexed for MEDLINE]
Free PMC Article
PubMed Commons home

PubMed Commons

0 comments
How to join PubMed Commons

    Supplemental Content

    Full text links

    Icon for HighWire Icon for PubMed Central
    Loading ...
    Support Center