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NCT Junior Research Group Bone Marrow Environment in Myeloid Malignancies

The focus of this junior research group is to understand the alterations in the bone marrow microenvironment in myeloid malignancies. Increasing evidence suggests a critical role of cell populations that form the hematopoietic stem cell niche, not only in normal hematopoiesis, but also in the initiation of myelodysplastic syndrome and the progression to leukemia. We focus in changes in cell adhesive interactions between hematopoietic progenitors and cells that form the hematopoietic niche.

Another aim of this group is to study alteration in cell metabolism of hematopoietic progenitors due to inflammation in health and myeloid malignancies. Our overall aim is to understand the complex interactions between cell populations in the bone marrow that promote disease pathogenesis.

Bone Marrow Environment in Myeloid Malignancies

(A) Schematic presentation of the normal hematopoietic stem niche. (B) Cell populations and biologic processes involved in MDS pathogenesis. (C) Flow cytometry analysis for the characterization of hematopoietic progenitors in the BM.
Copyright: Ioannis Mitroulis


Dr. Ioannis Mitroulis
Junior Group Leader
Phone: +49 (0)351 458 6250
Email: ioannis.mitroulis(at)uniklinikum-dresden.de

Dr. Ioannis Kourtzelis
Phone: +49 (0)351 458 6250
Email: ioannis.kourtzelis(at)uniklinikum-dresden.de


Mitroulis I, et al. Modulation of myelopoiesis progenitors is an integral component of trained immunity. Cell doi.10.1016/j.cell.2017.11.034

Mitroulis, I. et al. Secreted protein Del-1 regulates myelopoiesis in the hematopoietic stem cell niche. J. Clin. Invest. 127, 3624–3639 (2017).


Mitroulis, I. et al. Leukocyte integrins: role in leukocyte recruitment and as therapeutic targets in inflammatory disease. Pharmacol. Ther. 147, 123–135 (2015).

Shin, J. et al. DEL-1 restrains osteoclastogenesis and inhibits inflammatory bone loss in nonhuman primates. Sci. Transl. Med. 7, 307ra155 (2015).


Mitroulis, I. et al. Developmental endothelial locus-1 attenuates complement-dependent phagocytosis through inhibition of Mac-1-integrin. Thromb. Haemost. 111, 1004–1006 (2014).