Mara Pavel-Dinu
Seattle Children's Research Institute, University of Washington School of Medicine, Seattle, WA, Stanford University, University of California, Los Angeles, De Anza College
Research areas: Biochemistry, Genetics and Molecular Biology · Molecular Biology · CRISPR and Genetic Engineering · Virus-based gene therapy research · CAR-T cell therapy research
About
Dr. Mara Pavel-Dinu is a basic and translational scientist whose research seeks to understand how stress signals, such as metabolic, inflammatory, or ex vivo culture-related, shape hematopoietic stem cell (HSC) function and immune tolerance in children with inborn errors of immunity (IEI). Her work focuses on uncovering how long-term hematopoietic stem cells (LT-HSCs) normally sense and adapt to metabolic or inflammatory stress, how these adaptive responses break down in disease, and might be revived or therapeutically reprogrammed to restore regeneration and tolerance.
Her laboratory investigates how genome editing, oxygen tension, and metabolic remodeling influence stem cell survival, DNA repair, and the restoration of effective hematopoiesis and immune balance. By identifying mechanisms of stress adaptation and metabolic vulnerability, her team aims to engineer next-generation gene and cell therapy platforms that achieve curative, durable outcomes rather than incremental improvement. The lab also explores how innate-like immune cells, including invariant natural killer T (iNKT) cells, promote hematopoietic resilience and sustained immune equilibrium during chronic inflammation.
Dr. Pavel-Dinu earned her B.S. in Microbiology, Immunology, and Molecular Genetics at the University of California, Los Angeles. She completed her Ph.D. and postdoctoral training at Stanford University, where she developed genome-editing strategies for primary immunodeficiencies. During this time, she also initiated pioneering studies on how oxygen availability and cellular metabolism interact to influence hematopoietic outcomes, an area now gaining significant traction in the field.
In 2024, she was appointed Assistant Professor in the Department of Pediatrics, Division of Immunology, at the University of Washington School of Medicine, and joined the Seattle Children’s Research Institute as a Principal Investigator in the Center for Immunity and Immunotherapies (CIIT).
The Pavel-Dinu Lab is dedicated to advancing curative and equitable gene and cell therapies for children with inherited immune disorders, with a commitment to addressing complex disease phenotypes and enhancing representation of diverse populations historically underrepresented in genetic research.
Employment
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Seattle Children's Research Institute Principal Investigator2024 - Present
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University of Washington School of Medicine, Seattle, WA Assistant Professor2024 - Present
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Stanford University School of Medicine Instructor2021 - 2024
Education
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Stanford University School of Medicine Postgraduate Fellow2015 - 2021
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Stanford University School of Medicine Ph.D. Student/NSF Fellow2007 - 2015
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University of California Los Angeles Bachelor of Science2002 - 2004
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De Anza College Transfer student1999 - 2002
Projects & Funding
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Discovery of mechanisms supporting the long-term regenerative potential of CRISPR/Cas9-AAV6 genome-targeted hematopoietic stem cells. National Blood Foundation2022 - 2023
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Development of a 2nd generation-engineered Tr1 cell therapy SPARK2022 - 2024
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Gene Correction for RAG2-SCID Disorder in Human Hematopoietic Stem Cell Primary Immunodeficiency Training Consortium (NIH/NCATS-NIAID)2021 - 2023
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Graduate Student Research Fellowship National Science Foundation2010 - 2013
Publications (27)
- Epigenetic landscape, key transcriptional regulators, and in vivo identification of human Tr1 cells Save
- Correcting Autoinflammation in STING-Associated Vasculopathy with Onset in Infancy (SAVI) by Human Stem Cell Genome-Editing Save
- Genetically corrected RAG2-SCID human hematopoietic stem cells restore V(D)J-recombinase and rescue lymphoid deficiency Save
- International Society for Cell & Gene Therapy Stem Cell Engineering Committee: Cellular therapies for the treatment of graft-versus-host-disease after hematopoietic stem cell transplant Save
- Rare immune diseases paving the road for genome editing-based precision medicine. Save
- CRISPR-Cas9-AAV versus lentivector transduction for genome modification of X-linked severe combined immunodeficiency hematopoietic stem cells. Save
- Genetically Corrected RAG2-SCID Human Hematopoietic Stem Cells Restore V(D)J-Recombinase and Rescue Lymphoid Deficiency Save
- A Curative DNA Code for Hematopoietic Defects: Novel Cell Therapies for Monogenic Diseases of the Blood and Immune System. Save
- Correction to: Gene Editing Rescues in Vitro T Cell Development of RAG2-Deficient Induced Pluripotent Stem Cells in an Artificial Thymic Organoid System. Save
- Enhanced homology-directed repair for highly efficient gene editing in hematopoietic stem/progenitor cells. Save
- Correction of X-CGD patient HSPCs by targeted CYBB cDNA insertion using CRISPR/Cas9 with 53BP1 inhibition for enhanced homology-directed repair. Save
- Gene Editing Rescues In vitro T Cell Development of RAG2-Deficient Induced Pluripotent Stem Cells in an Artificial Thymic Organoid System. Save
- Improved Genome Editing through Inhibition of FANCM and Members of the BTR Dissolvase Complex. Save
- Author Correction: Gene correction for SCID-X1 in long-term hematopoietic stem cells. Save
- High-efficiency CRISPR induction of t(9;11) chromosomal translocations and acute leukemias in human blood stem cells. Save
- Highly Efficient and Marker-free Genome Editing of Human Pluripotent Stem Cells by CRISPR-Cas9 RNP and AAV6 Donor-Mediated Homologous Recombination. Save
- Author Correction: Gene correction for SCID-X1 in long-term hematopoietic stem cells. Save
- Gene correction for SCID-X1 in long-term hematopoietic stem cells. Save
- Identification of preexisting adaptive immunity to Cas9 proteins in humans. Save
- A high-fidelity Cas9 mutant delivered as a ribonucleoprotein complex enables efficient gene editing in human hematopoietic stem and progenitor cells. Save