NDLI: Hoxa9 and Flt3 signaling synergistically regulate an early checkpoint in lymphopoiesis.

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Hoxa9 and Flt3 signaling synergistically regulate an early checkpoint in lymphopoiesis.

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Hoxa9 and Flt3 signaling synergistically regulate an early checkpoint in lymphopoiesis.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Medina, Kay L. Gwin, Kimberly A. Dolence, Joseph J. Shapiro, Mariya B. Huang, Zhixin L.
Description	Country affiliation: United States Author Affiliation: Gwin KA ( Department of Immunology, Mayo Clinic, Rochester, MN 55905, USA.)
Abstract	Hoxa9 and Flt3 signaling are individually important for the generation of lymphoid lineage precursors from multipotent hematopoietic progenitors (MPP) in bone marrow. Mice deficient for Hoxa9, Flt3, or Flt3 ligand (FL) have reduced numbers of lymphoid-primed multipotential progenitors (LMPP), common lymphoid progenitors (CLP), and B/T cell precursors. Hoxa9 regulates lymphoid development, in part, through transcriptional regulation of Flt3. However, it was unclear whether Hoxa9 has functions in lymphopoiesis independent of, or alternatively, synergistically with Flt3 signaling. In this study, we show that Hoxa9(-/-)Flt3l(-/-) mice have more severe deficiencies in all B lineage cells, CLP, LMPP, and total Flt3(+) MPP in bone marrow than the single knockouts. Although LMPP and Flt3(+) CLP contain precursors for NK and dendritic cell lineage cells, no deficiencies in these lineages beyond that in Flt3l(-/-) mice was found. Thymocyte cellularity was significantly reduced in the compound knockout, although peripheral T cell numbers mirrored Flt3l(-/-) mice. Analysis of the hematopoietic progenitor compartment revealed elevated numbers of CD150(+hi)CD34(-)CD41(+) myeloid-biased stem cells in Hoxa9(-/-)Flt3l(-/-) mice. In contrast, CD150(-) MPP enriched for lymphoid potential were synergistically reduced, suggesting Hoxa9 and Flt3 signaling function coordinately to regulate lymphopoiesis at a very early stage. Real-time PCR analysis of CD150(-)Flt3(+) cells from wild-type control, Hoxa9(-/-), and Flt3l(-/-) single knockouts revealed decreased lymphoid transcripts, corroborating the importance of these regulators in lymphoid development. Taken together, these studies reveal a very early checkpoint in lymphopoiesis dependent on the combinatorial activities of Hoxa9 function and Flt3 signaling.
ISSN	00221767
e-ISSN	15506606
DOI	10.4049/jimmunol.1203294
Journal	The Journal of Immunology
Issue Number	2
Volume Number	191
Language	English
Publisher	The American Association of Immunologists
Publisher Date	2013-07-15
Publisher Place	United States
Access Restriction	Open
Subject Keyword	Homeodomain Proteins Metabolism Lymphoid Progenitor Cells Cytology Lymphopoiesis Fms-like Tyrosine Kinase 3 Animals Antigens, Cd Antigens, Cd34 B-lymphocytes Immunology Bone Marrow Cells Cell Differentiation Cell Lineage Dendritic Cells Granulocyte-macrophage Progenitor Cells Genetics Killer Cells, Natural Lymphocyte Count Membrane Proteins Mice Mice, Inbred C57bl Mice, Knockout Platelet Membrane Glycoprotein Iib Receptors, Cell Surface Signal Transduction Transcription, Genetic Research Support, N.i.h., Extramural Discipline Immunology
Content Type	Text
Resource Type	Article
Subject	Immunology and Allergy Immunology

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Hoxa9 and Flt3 signaling synergistically regulate an early checkpoint in lymphopoiesis.