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 Blood, 15 November 2008, Vol. 112, No. 10, pp. 4080-4089.
Prepublished online as a Blood First Edition Paper on August 27, 2008; DOI 10.1182/blood-2008-03-143776.

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Submitted March 6, 2008
Accepted August 10, 2008

Mononuclear Myeloid-Derived "Suppressor" Cells express RAE-1 and activate NK cells

Norman Nausch, Ioanna E Galani, Eva Schlecker, and Adelheid Cerwenka*

Innate Immunity, German Cancer Research Center, Heidelberg, Germany

* Corresponding author; email: a.cerwenka{at}dkfz.de.

Myeloid-Derived Suppressor Cells (MDSC) accumulate in cancer patients and tumor-bearing mice and potently suppress T cell activation. In this study, we investigated whether MDSC regulate NK cell function. We discovered that mononuclear Gr-1+CD11b+F4/80+ MDSC isolated from RMA-S tumor-bearing mice do not suppress, but activate NK cells to produce high amounts of IFN-{gamma}. Gr-1+CD11b+F4/80+ MDSC isolated from tumor-bearing mice, but not myeloid cells from naive mice, expressed the ligand for the activating receptor NKG2D, RAE-1. NK cell activation by MDSC depended partially on the interaction of NKG2D on NK cells with RAE-1 on MDSC. NK cells eliminated Gr-1+CD11b+F4/80+ MDSC in vitro and upon adoptive transfer in vivo. Finally, depletion of Gr-1+ cells that comprise MDSC confirmed their protective role against the NK-sensitive RMA-S lymphoma in vivo. Our study reveals that MDSC do not suppress all aspects of anti-tumor immune responses and defines a novel, unexpected activating role of MDSC on NK cells. Thus, our results have great impact on the design of immune therapies against cancer aiming at the manipulation of MDSC.


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