Jeffrey Bednarski, MD, PhD


Jeff-BednarskiI grew up in northwest Pennsylvania and attended Duke University for my undergraduate studies.  I then received my M.D. and Ph.D. from the University of Michigan School of Medicine where I conducted my graduate research in new treatments for autoimmune diseases with Gary Glick. I completed my residency in Pediatrics at St. Louis Children’s Hospital and my fellowship in Pediatric Hematology-Oncology at Washington University School of Medicine.  During my fellowship, I worked with Dr. Barry Sleckman in the Department of Pathology and Immunology on the role of DNA damage responses in early immune development.  After joining faculty at Washington University, I continued my research in immunology in addition to my clinical activities in pediatric oncology and bone marrow transplantation.  My clinical interests are in immunological complications related to hematological disorders and bone marrow transplantation for immune deficiencies.


The Bednarski lab investigates signaling networks that regulate hematopoiesis and lymphopoiesis and how alterations in these pathways lead to immune deficiencies or transformation into lymphoid malignancy. In particular, we’re interested in how signals from DNA damage cooperate with other developmental processes to direct hematopoietic cell differentiation and survival. During early immune development, lymphocytes must intentionally generate and repair breaks in their antigen receptor genes to assemble a diverse antibody repertoire. We are investigating how signals from these DNA breaks trigger cellular programs that direct lymphocyte differentiation and prevent leukemic transformation. Additionally, we are interested in understanding how cells distinguish between these normal, programmed DNA breaks and deleterious DNA damage from genotoxic sources (such as chemotherapy or radiation therapy) to appropriately direct development versus cell death, respectively. We’re also interested in understanding how errors in DNA damage responses lead to aberrant immune development and immune deficiencies.

Recent publications

  1. Bednarski JJ, Nickless A, Bhattacharya D, Amin RH, Schlissel MS, Sleckman BP. RAG-induced DNA double-strand breaks signal through Pim2 to promote pre-B cell survival and limit proliferation. J. Exp. Med. 2012; 209:11-7.
  2. Bednarski JJ, Pandey R, Schulte E, White LS, Chen BR, Sandoval GJ, Kohyama M, Haldar M, Nickless A, Trott A, Cheng G, Murphy KM, Bassing CH, Payton JE, Sleckman BP. RAG-mediated DNA double-strand breaks activate a cell type-specific checkpoint to inhibit pre-B cell receptor signals. J Exp Med. 2016;213(2):209-23.
  3. Fistonich C, Zehentmeier S, Bednarski JJ, Miao R, Schjerven H, Sleckman BP, Pereira JP. Cell circuits between B cell progenitors and IL-7+ mesenchymal progenitor cells control B cell development. J Exp Med. 2018;215(10):2586-2599.
  4. Soodgupta D, White LS, Yang W, Johnston R, Andrews JM, Kohyama M, Murphy KM, Mosammaparast N, Payton JE, Bednarski JJ. RAG-Mediated DNA Breaks Attenuate PU.1 Activity in Early B Cells through Activation of a SPIC-BCLAF1 Complex. Cell Rep. 2019;29(4):829-843.e5.
  5. Bednarski JJ, Sleckman BP. At the intersection of DNA damage and immune responses. Nat Rev Immunol. 2019;19(4):231-242.
  6. Greenberg ZJ, Monlish DA, Bartnett RL, Yang Y, Shen G, Li W, Bednarski JJ, Schuettpelz LG. The Tetraspanin CD53 Regulates Early B Cell Development by Promoting IL-7R Signaling. J Immunol. 2020;204(1):58-67.
  7. Collins PL, Purman C, Porter SI, Nganga V, Saini A, Hayer KE, Gurewitz GL, Sleckman BP, Bednarski JJ, Bassing CH, Oltz EM. DNA double-strand breaks induce H2Ax phosphorylation domains in a contact-dependent manner. Nat Commun. 2020;11(1):3158.