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Flt3 Ligand Regulates Dendritic Cell Development from Flt3+ Lymphoid and Myeloid-committed Progenitors to Flt3+ Dendritic Cells In Vivo

Flt3 Ligand Regulates Dendritic Cell Development from Flt3+ Lymphoid and Myeloid-committed... Stimulation of Flt3 receptor tyrosine kinase through its cognate ligand expands early hematopoietic progenitor and dendritic cells (DCs) in humans and mice. The exact developmental stages at which hematopoietic progenitors express Flt3, are responsive to its ligand, and subsequently develop to DCs, are not known. Here we show that common lymphoid and common myeloid progenitors, as well as steady state DCs in thymus, spleen, and epidermis, express Flt3. The receptor is down-regulated once definitive B cell, T cell, and megakaryocyte/erythrocyte commitment occurs, and Flt3 is not detectable on other steady state hematopoietic cell populations. Upon in vivo Flt3 ligand (Flt3L) administration, Flt3 + progenitor cells and their progeny DCs are expanded, whereas Flt3 − downstream progenitors are not, or are only slightly increased. Transplantation of common lymphoid and common myeloid progenitors and subsequent Flt3L injection increases progeny DCs of both precursor populations. These findings provide a definitive map of Flt3 expression in the hematopoietic hierarchy and directly demonstrate that Flt3L can drive DC development along both the lymphoid and myeloid developmental pathways from Flt3 + progenitors to Flt3 + DCs. Flt3/Flt3L dendritic cells development hematopoietic progenitors Footnotes ↵ * Abbreviations used in this paper: CLP, common lymphoid progenitor; CMP, common myeloid progenitor; Flt3L, Flt3 ligand; GMP, granulocyte/macrophage progenitor; HSC, hematopoietic stem cell; IPC, interferon α–producing cell; MEP, megakaryocyte/erythrocyte progenitor; SLF, steel factor. Submitted: 27 February 2003 Accepted: 14 May 2003 Revision received 14 May 2003 http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png The Journal of Experimental Medicine Rockefeller University Press

Flt3 Ligand Regulates Dendritic Cell Development from Flt3+ Lymphoid and Myeloid-committed Progenitors to Flt3+ Dendritic Cells In Vivo

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References (45)

Publisher
Rockefeller University Press
Copyright
© 2003 Rockefeller University Press
ISSN
0022-1007
eISSN
1540-9538
DOI
10.1084/jem.20030323
pmid
12874263
Publisher site
See Article on Publisher Site

Abstract

Stimulation of Flt3 receptor tyrosine kinase through its cognate ligand expands early hematopoietic progenitor and dendritic cells (DCs) in humans and mice. The exact developmental stages at which hematopoietic progenitors express Flt3, are responsive to its ligand, and subsequently develop to DCs, are not known. Here we show that common lymphoid and common myeloid progenitors, as well as steady state DCs in thymus, spleen, and epidermis, express Flt3. The receptor is down-regulated once definitive B cell, T cell, and megakaryocyte/erythrocyte commitment occurs, and Flt3 is not detectable on other steady state hematopoietic cell populations. Upon in vivo Flt3 ligand (Flt3L) administration, Flt3 + progenitor cells and their progeny DCs are expanded, whereas Flt3 − downstream progenitors are not, or are only slightly increased. Transplantation of common lymphoid and common myeloid progenitors and subsequent Flt3L injection increases progeny DCs of both precursor populations. These findings provide a definitive map of Flt3 expression in the hematopoietic hierarchy and directly demonstrate that Flt3L can drive DC development along both the lymphoid and myeloid developmental pathways from Flt3 + progenitors to Flt3 + DCs. Flt3/Flt3L dendritic cells development hematopoietic progenitors Footnotes ↵ * Abbreviations used in this paper: CLP, common lymphoid progenitor; CMP, common myeloid progenitor; Flt3L, Flt3 ligand; GMP, granulocyte/macrophage progenitor; HSC, hematopoietic stem cell; IPC, interferon α–producing cell; MEP, megakaryocyte/erythrocyte progenitor; SLF, steel factor. Submitted: 27 February 2003 Accepted: 14 May 2003 Revision received 14 May 2003

Journal

The Journal of Experimental Medicine – Rockefeller University Press

Published: Jul 21, 2003

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