Ivan Maillard, MD, PhD
Ivan Maillard’s main interest is to investigate the signals regulating the development and function of blood-forming stem cells. He studies the specialized microenvironment that nurtures blood-forming stem cells, using the mouse as a model organism.
In particular, Dr. Maillard investigates how these cells are supported in fetal hematopoietic organs, such as the fetal liver, the main site of blood development during fetal life before migration of blood-forming stem cells into the bone marrow. Understanding these interactions will lead to novel strategies to expand blood-forming stem cells in culture or to enhance their function after transplantation. In addition, it might provide insights into the function of stem cells in other contexts, including in cancerous tissues.
Another interest of the Maillard laboratory is in the self-renewal and differentiation of mature T lymphocytes, a subset of lymphocytes that plays a critical role in immunization, anti-cancer responses and diseases such as AIDS and autoimmune disorders.
Dr. Maillard earned his MD at the University of Lausanne, Switzerland and a PhD in Immunology from the MD-PhD program of the Swiss Academy of Medical Sciences. His graduate work with Heidi Diggelmann, MD, aimed at understanding the complex interaction of mouse retroviruses with the immune system of their host. He subsequently completed a post-doctoral fellowship with Warren S. Pear at the University of Pennsylvania, where he also worked as an instructor and physician in Hematology-Oncology. There, Maillard investigated the role of signals delivered by the Notch pathway in the development of lymphocytes and in the homeostasis of blood-forming stem cells. His work was supported by a fellowship from the Damon Runyon Cancer Research Foundation.
He joined the Life Sciences Institute as a Research Assistant Professor and is affiliated with the U-M Center for Stem Cell Biology. He is also an Assistant Professor in the Department of Internal Medicine, Division of Hematology/Oncology.
Notch signaling, hematopoietic stem cells, leukemia, T cell differentiation and homeostasis, bone marrow transplantation, alloimmunity
Jones M, Bisht K, Savage SA, Nandakumar J, Keegan CE, Maillard I. The Shelterin Complex and Hematopoiesis. J Clin Invest, in press.
Jones M*, Chase J*, Brinkmeier M, Xu J, Weinberg DN, Schira J, Friedman A, Malek S, Grembecka J, Cierpicki T, Dou Y, Camper SA, Maillard I. Ash1l controls quiescence and self-renewal potential in hematopoietic stem cells. J Clin Invest, 125(5): 2007-2020, 2015. (*equal contribution)
Pinnell N, Yan R, Cho HJ, Keeley T, Murai MJ, Liu Y, Serna Alarcon A, Qin J, Qang Q, Kuick R, Elenitoba-Johnson KSJ, Maillard I, Samuelson LC, Cierpicki T, Chiang MY. The PIAS-like coactivator Zmiz1 is a direct and selective cofactor of Notch1 in T cell development and leukemia. Immunity, 43(5): 870-883, 2015.
Borkin D, He S, Miao H, Kempinska K, Pollock J, Chase J, Malik B, Purohit T, Zhao T, Wang J, Wen B, Zong H, Jones M, Danet-Desnoyers G, Guzman ML, Talpaz M, Bixby DL, Sun D, Hess JL, Muntean AG, Maillard I, Cierpicki T, Grembecka J. Pharmacologic inhibition of the menin-MLL interaction blocks progression of MLL leukemia in vivo. Cancer Cell, 27(4): 589-602, 2015.
Wood S, Feng J, Chung J, Radojcic V, Sandy AR, Friedman A, Shelton A, Yan M, Siebel CW, Bishop DK, Maillard I. Transient blockade of Delta-like Notch ligands prevents allograft rejection mediated by cellular and humoral mechanisms in a mouse model of heart transplantation. J Immunol, 194(6): 2899-2908, 2015.
Kocak H, Ballew BJ, Bisht K, Eggebeen R, Hicks BD, Suman S, O’Neil A, Giri N, NCI DCEG Cancer Genomics Research laboratory, NCI DCEG Cancer Sequencing Working Group, Maillard I, Alter BP, Keegan CE, Nandakumar J, Savage SA. Hoyeraal-Hreidarsson syndrome caused by a germline mutation in the TEL patch of the telomere protein TPP1. Genes and Development, 28(19): 2090-2102, 2014.
Jones M, Osawa G, Regal JA, Weinberg DN, Taggart J, Kocak H, Friedman A, Ferguson DO, Keegan CE, Maillard I. Hematopoietic stem cells are acutely sensitive to Acd shelterin gene inactivation. J Clin Invest 124(1): 353-366, 2014.
Muntean AG, Chen W, Jones M, Granowicz EM, Maillard I, Hess JL. MLL fusion protein-driven AML is selectively inhibited by targeted disruption of the MLL-PAFc interaction. Blood 122(11):1914-1922, 2013.
Ebens CE, Maillard I. Notch signaling in hematopoietic cell transplantation and T cell alloimmunity. Blood Reviews 27(6): 269-277, 2013.
Sandy AR, Stoolman J, Malott K, Pongtornpipat P, Segal BM, Maillard I. Notch signaling regulates T cell accumulation and function in the central nervous system during experimental autoimmune encephalomyelitis. J Immunol, 191(4): 1606-1613, 2013.