Macrophage Specification and Biology Through the Lens of Forced Cell Fate Transitions
Time
3:00 PM, July 21, 2026 (Beijing)9:00 AM, July 21, 2026 (Barcelona)
Zoom Meeting Link: https://us06web.zoom.us/j/82575240179?pwd=4OTaFlw8zLIqi4EgCxSuRvZ2zjMI68.1
Meeting ID: 825 7524 0179
Passcode: 810914
Contact Us
Email: mcjournal@sciexplor.comSpeaker
Prof. Thomas Graf
Centre for Genomic Regulation (CRG), The Barcelona Institute of Science and Technology, Barcelona, Spain.
Thomas Graf, born in Vienna and raised in Germany and Venezuela, is an Emeritus at the Centre for Genomic Regulation (since 2025) in Barcelona, where he has been based since 2006. He previously held senior research positions at the Albert Einstein College of Medicine, the European Molecular Biology Laboratory in Heidelberg, the German Cancer Research Center, and the Max Planck Institute in Tübingen.
His research began with avian acute leukemia viruses, where he showed that multiple viral oncogenes cooperate in leukemia and that oncogenes can drive disease by blocking differentiation. He later focused on how hematopoietic stem cells commit to specialized lineages and on the role of transcription factors in this process. In the 1990s and 2000s, he demonstrated that single transcription factors can trigger transdifferentiation between hematopoietic lineages, opening new ways to study cell fate. More recently, his group showed that C/EBPalpha can enhance reprogramming into iPS cells, suggesting broader roles in early development. His work has advanced fundamental understanding of differentiation and supported new medical applications.
Prof. Graf has received numerous national and international awards, organized major conferences, served on editorial boards of numerous journals, and is an elected member of EMBO and Academia Europaea.
His research began with avian acute leukemia viruses, where he showed that multiple viral oncogenes cooperate in leukemia and that oncogenes can drive disease by blocking differentiation. He later focused on how hematopoietic stem cells commit to specialized lineages and on the role of transcription factors in this process. In the 1990s and 2000s, he demonstrated that single transcription factors can trigger transdifferentiation between hematopoietic lineages, opening new ways to study cell fate. More recently, his group showed that C/EBPalpha can enhance reprogramming into iPS cells, suggesting broader roles in early development. His work has advanced fundamental understanding of differentiation and supported new medical applications.
Prof. Graf has received numerous national and international awards, organized major conferences, served on editorial boards of numerous journals, and is an elected member of EMBO and Academia Europaea.
Host
Prof. Florent Ginhoux
Singapore Immunology Network (SIgN), Agency for Science, Technology and Research (A*STAR), Singapore, Singapore.
Florent Ginhoux, PhD, is Senior Principal Investigator at the Singapore Immunology Network (SIgN), A*STAR, Singapore. He studies the ontogeny, differentiation, and functional specialization of dendritic cells, monocytes, and macrophages.
His research focuses on tissue-resident myeloid cells in both humans and mice, using approaches such as RNA sequencing, single-cell transcriptomics, flow cytometry, and CyTOF to characterize their heterogeneity and developmental pathways.
His recent work investigates how myeloid cell ontogeny shapes their functions in tissue homeostasis, immunity, and inflammation, with the aim of advancing understanding of myeloid biology and informing therapeutic strategies in human disease.
His research focuses on tissue-resident myeloid cells in both humans and mice, using approaches such as RNA sequencing, single-cell transcriptomics, flow cytometry, and CyTOF to characterize their heterogeneity and developmental pathways.
His recent work investigates how myeloid cell ontogeny shapes their functions in tissue homeostasis, immunity, and inflammation, with the aim of advancing understanding of myeloid biology and informing therapeutic strategies in human disease.
Introduction
In this lecture, I will provide an overview of our work on macrophage specification and cell fate plasticity, beginning with v-Myb as a viral oncogene that induces early myeloid cell proliferation and macrophage dedifferentiation. I will then discuss the use of v-Myb-Ets leukemia virus-transformed avian leukemia cells as a surrogate stem cell model represented by a myeloid-erythroid-thrombocytic progenitor, followed by examples of lineage plasticity in committed cells, including PU.1-driven myeloid differentiation of erythroid progenitors and the PU.1-GATA1 cross-antagonism concept. Next, I will present a powerful transdifferentiation system in which CEBPa converts normal and leukemic B cells into macrophages in a PU.1-dependent manner, and highlight how B cell rewiring by CEBPa occurs at multiple levels. I will also discuss evidence that induced macrophage transdifferentiation proceeds through a myeloid progenitor state without requiring cell division. Finally, I will address the reprogramming of tumor cells into antigen-presenting cells as a novel anti-cancer therapy approach.
