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Blood, 15 February 2006, Vol. 107, No. 4, pp. 1445-1453.
Prepublished online as a Blood First Edition Paper on October 13, 2005; DOI 10.1182/blood-2005-04-1721.
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Submitted April 27, 2005
Accepted September 30, 2005
Differential involvement of PU.1 and Id2 downstream of TGF- 1 during Langerhans cell commitment
Leonhard X Heinz, Barbara Platzer, Peter M Reisner, Almut Jorgl, Sabine Taschner, Florian Gobel, and Herbert Strobl*
Institute of Immunology, Medical University Vienna, Vienna, Austria
* Corresponding author; email: herbert.strobl{at}meduniwien.ac.at.
Langerhans cells (LCs) are highly abundant dendritic cells (DCs) in epidermal and mucosal tissues. The transcription factors PU.1 and Id2 have been implicated as positive regulators of LC development from hematopoietic progenitor cells. LC differentiation from progenitors is absolutely dependent on transforming growth factor beta 1 (TGF- 1) in vitro as well as in vivo, however downstream mechanisms are poorly defined. We found that both PU.1 and Id2 are induced by TGF-1 in human CD34+ monocyte/LC (M/LC) progenitor cells, and that neither ectopic PU.1 or Id2 alone, nor both together, could replace TGF-1 in its instructive function on LC commitment. However, both factors critically contributed to LC differentiation by acting at two distinct intersection points. Ectopic PU.1 strongly enhanced TGF-1-dependent LC development. Additionally, also Notch-induced generation of interstitial-type DCs was associated with PU.1 upregulation. Thus PU.1 is generally increased during myeloid DC development. Ectopic Id2 inhibits the acquisition of early monocytic characteristics by cells generated in the absence of TGF-1, and also inhibited monocyte induction by alternative stimuli. Since TGF-1 represses a default monocyte pathway of common progenitor cells, PU.1 and Id2 seem to modulate lineage options of M/LC precursors, downstream of TGF-1.
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