Ivan Maillard

Our Research

Please note, the Maillard lab is transitioning to the Perelman School of Medicine at the University of Pennysylvania.

The Maillard laboratory is interested in the study of blood-forming stem cells, blood cell development and the development and function of T lymphocytes. Our research is devoted to the following main topics: 1) Understanding the role of Notch signaling in the regulation of T cell homeostasis and differentiation, particularly in the setting of allogeneic T cell responses; 2) investigating the homeostasis of blood-forming stem cells in situations of hematopoietic stress and the role of epigenetic regulation in their regulation. In a first project, we are interested in the regulation of mature T cell homeostasis and differentiation by Notch signaling. Using several genetic models of Notch inactivation, we are investigating the molecular and cellular mechanisms underlying the activity of Notch signaling in allogeneic T cell responses (T cell responses against foreign tissue antigens). Our findings indicate that Notch behaves as a novel and potent master regulator of T cell function in several mouse models of graft-versus-host disease. We are currently investigating the molecular mechanisms of this effect and exploring its potential therapeutic applications.

About Ivan Maillard

  • Oncology
  • Hematology
  • Stem cells

Ivan Maillard, a member of the U-M Center for Stem Cell Biology, investigates the interaction of blood-forming stem cells with their environment. Also a practicing oncologist, Dr. Maillard's research focuses on characterizing the mechanisms that regulate the maintenance of stem cells at different stages of development, knowledge that may provide insight into diseases such as leukemia and other cancers.

Research highlight: Graft-vs.-host disease

Ivan Maillard found that inhibiting a signaling pathway in some of the transplanted cells in bone-marrow transplants could prevent the most serious potential complications of the procedure: a conflict between the transplanted cells and the recipient’s own tissue called graft-versus-host disease. Antibodies inhibiting specific elements of a cell-to-cell communication pathway called Notch signaling prevented graft-versus-host disease in mice—without serious side effects and without substantially compromising the cancer-fighting ability of the transplanted cells. The research was published in the Journal of Clinical Investigation on March 1, 2013.

Recent publications

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, Apr 13, 2015 [Epub ahead of print]. Wood S, Feng J, Chung J, Radojcic V, Sandy-Sloat 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. 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. 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. Tran IT, Sandy AR, Carulli AJ, Ebens C, Chung J, Shan GT, Radojcic V, Friedman A, Gridley T, Shelton A, Reddy P, Samuelson LC, Yan M, Siebel CW, Maillard I. Blockade of individual Notch ligands and receptors controls graft-versus-host disease. J Clin Invest. 2013, 123(4): 1590-1604, 2013.