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Professor Allison Pettit
Professor

Allison Pettit

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Overview

Background

Professor Pettit leads the Bones and Immunology Research Group at Mater Research Institute-UQ and is Director of Biomedical Research for Mater Research. Professor Pettit has led multidisciplinary research discovering intersecting biological mechanisms across the fields of immunology, rheumatology, cancer biology, haematology and bone biology. Professor Pettit is currently a UQ Amplify recipient associated with an ARC Future Fellowship, 2017-2020 and CIA on an NHMRC Ideas Grant, 2022-25. Major contributions led by Professor Pettit include the paradigm shifting discovery of a novel population of resident macrophages, osteal macrophages (osteomacs), and their role in promoting bone formation and bone regeneration after injury. Her team have published over 17 manuscripts based on this original discovery (with over 1700 citations) including translation of this basic research discovery toward eluciating novel disease mechanism from cancer bone metastasis to osteoporosis. This also led to the novel discovery of bone marrow resident macrophage contributions to supporting blood stem cells niches and the key role that these cells play in protecting this vital niche from cancer therapies. Bone marrow and specifically haematopoietic stem cell damage is one of the most serious and life-threatening side effects of cancer therapies. Here discoveries are cited in over 117 patent documents and she is currently collaborating with a major pharmaceutical partner.

Professor Pettit's leadership and achievements have been recognised through multiple awards including the 2019 UQ Faculty of Medicine Leader of the Year (Academic), Women in Technology 2018 Life Sciences Outstanding Achievement Award and becoming a Fellow of the American Society of Bone and Mineral Research. Professor Pettit has been invited to give numerous presentations at national and international conferences including Seoul Symposium on Bone Health, Asia-Pacific League of Associations for Rheumatology Congress and a prestigious American Society of Bone and Mineral Research Meet-the-Professor session. Professor Pettit is and Associate Editor for the Journal of Bone and Mineral Research, is an past Council member for the Australian and New Zealand Bone and Mineral Society, and chairs or serves on numerous committees including the Association of Australian Medical Research Institutes Gender Equity, Diversity and Inclusion Committee. PhD candidates under Professor Pettit's supervision have all been supported by scholarships (including 2 x NHMRC), received numerous local and national awards (e.g. Dr Alexander, ASMR QLD Premier Postgraduate Award, 2011 and Dr Lena Batoon won the UQ Faculty of Medicine Graduate of the Year Award, 2021), all had high quality first author publications at completion and 2 received UQ Dean’s Commendations.

Availability

Professor Allison Pettit is:
Available for supervision
Media expert

Qualifications

  • Bachelor (Honours) of Science (Advanced), Griffith University
  • Doctor of Philosophy, The University of Queensland

Research impacts

  • Discovery that the transcription factor RelB is a critical molecular mediator of dendritic cell antigen presentation and extended this to show that RelB expressing dendritic cells have critical roles in the initiation and perpetuation of joint inflammation in inflammatory arthritis. These discoveries were used by my principal HDR supervisor (Professor Ranjeny Thomas; https://researchers.uq.edu.au/researcher/396) as the knowledge platform to develop the first vaccine therapy for rheumatoid arthritis.
  • Demonstration that RANKL is the essential and rate limiting cytokine required for osteoclast formation and focal bone erosion in inflammatory arthritis. This research output influenced pharmaceutical industry development of the blockbuster drug Denosumab.
  • Leadership of the paradigm shifting discovery of a novel population of resident macrophages, osteal macrophages (osteomacs), and their novel role in promoting osteoblastic bone formation and bone regeneration after injury. This has completely changed how the bone and mineral/orthopaedic research field views macrophage contributions to bone health and disease and has influence parallel fields including tissue regeneration and biomaterials.
  • Discovery that macrophages regulate haematopoietic stem cell (HSC) niche homeostasis. The landmark paper on which I am co-first author is a Web of Science highly cited paper (top 1% or research outputs) that has been cited by papers spanning 46 research fields. We have since extended this discovery to demonstrate that resident macrophage resilience to lethal radiation is essential for bone marrow recovery and successful HSC engraftment and haematopoietic reconstitution post-HSC transplantation (senior author manuscript in Blood, 2018).
  • Exposed that resident tissue macropahges are fragmented during tissue single cell suspension generation, leaving behind encapsulated remnants of themselves that have detectable cell membrane proteins, intracellur proteins and reporter molecules and RNAs. This undermindes the accuracy of burgeoning high parameter technologies focussed on single cell analysis (e.g. flow cytometry, single cell RNAseq, CITESeq, etc) as depending on the tissue disaggregation and analysis strategy, macrophages are under-represented relative to their abundance in tissues and/or macrophage-expressed genes are mistakenly attributed to non-macrophage cells and vice versa

Works

Search Professor Allison Pettit’s works on UQ eSpace

150 works between 1996 and 2025

81 - 100 of 150 works

2010

Journal Article

Bone marrow macrophages maintain hematopoietic stem cell (HSC) niches and their depletion mobilizes HSCs

Winkler, Ingrid G., Sims, Natalie A., Pettit, Allison R., Barbier, Valérie, Nowlan, Bianca, Helwani, Falak, Poulton, Ingrid J., van Rooijen, Nico van, Alexander, Kylie A., Raggatt, Liza J. and Levesque, Jean-Pierre (2010). Bone marrow macrophages maintain hematopoietic stem cell (HSC) niches and their depletion mobilizes HSCs. Blood, 116 (23), 4815-4828. doi: 10.1182/blood-2009-11-253534

Bone marrow macrophages maintain hematopoietic stem cell (HSC) niches and their depletion mobilizes HSCs

2010

Journal Article

An antibody against the colony-stimulating factor 1 receptor (CSF1R) depletes the resident subset of monocytes and tissue and tumor-associated macrophages but does not inhibit inflammation

MacDonald, Kelli P. A., Palmer, James S., Cronau, Stephen, Seppanen, Elke Jane, Olver, Stuart, Raffelt, Neil C., Kuns, Rachel, Pettit, Allison R., Clouston, Andrew, Wainwright, Brandon J., Branstetter, Dan, Smith, Jeffrey, Paxton, Raymond J., Cerretti, Douglas Pat, Bonham, Lynn, Hill, Geoffrey R. and Hume, David A. (2010). An antibody against the colony-stimulating factor 1 receptor (CSF1R) depletes the resident subset of monocytes and tissue and tumor-associated macrophages but does not inhibit inflammation. Blood, 116 (19), 3955-3963. doi: 10.1182/blood-2010-02-266296

An antibody against the colony-stimulating factor 1 receptor (CSF1R) depletes the resident subset of monocytes and tissue and tumor-associated macrophages but does not inhibit inflammation

2010

Journal Article

Soluble lymphotoxin is an important effector molecule in GVHD and GVL

Markey, KA, Burman, AC, Banovic, T, Kuns, RD, Raffelt, NC, Rowe, V, Olver, SD, Don, ALJ, Morris, ES, Pettit, AR, Wilson, YA, Robb, RJ, Randall, LM, Korner, H, Engwerda, CR, Clouston, AD, MacDonald, KPA and Hill, GR (2010). Soluble lymphotoxin is an important effector molecule in GVHD and GVL. Blood, 115 (1), 122-132. doi: 10.1182/blood-2009-01-199927

Soluble lymphotoxin is an important effector molecule in GVHD and GVL

2010

Conference Publication

DEPLETION OF BONE MARROW PHAGOCYTES CAUSES THE MOBILIZATION OF LONG-TERM RECONSTITUTING HEMATOPOIETIC STEM CELLS

Jacobsen, RN, Levesque, JP, Barbier, V, Raggatt, LJ and Pettit, AR (2010). DEPLETION OF BONE MARROW PHAGOCYTES CAUSES THE MOBILIZATION OF LONG-TERM RECONSTITUTING HEMATOPOIETIC STEM CELLS. 39th Annual Scientific Meeting of the ISEH - Society-for-Hematology-and-Stem-Cells, Melbourne AUSTRALIA, SEP 15-18, 2010. NEW YORK: ELSEVIER SCIENCE INC.

DEPLETION OF BONE MARROW PHAGOCYTES CAUSES THE MOBILIZATION OF LONG-TERM RECONSTITUTING HEMATOPOIETIC STEM CELLS

2010

Conference Publication

Both DKK-1 and sost are suppressed during late stage disease development in a mouse model of ankylosing spondylitis

Thomas, G., Duan, R., Pettit, A., Glant, T. and Brown, M. (2010). Both DKK-1 and sost are suppressed during late stage disease development in a mouse model of ankylosing spondylitis. Seventh International Congress on Spondyloarthropathies, Gent, Belgium, 7 - 9 October 2010. Ospedaletto, PI, Italy: Pacini Editore SpA.

Both DKK-1 and sost are suppressed during late stage disease development in a mouse model of ankylosing spondylitis

2009

Journal Article

Responses in vivo to purified poly (3-hydroxybutyrate-co-3-hydroxyvalerate) implanted in a murine tibial defect model

Wu, A. C. K., Pettit, A. R., Toulson, S., Grondahl, L., Mackie, E. J. and Cassady, A. I. (2009). Responses in vivo to purified poly (3-hydroxybutyrate-co-3-hydroxyvalerate) implanted in a murine tibial defect model. Journal of Biomedical Materials Research Part A, 91A (3), 845-854. doi: 10.1002/jbm.a.32238

Responses in vivo to purified poly (3-hydroxybutyrate-co-3-hydroxyvalerate) implanted in a murine tibial defect model

2009

Journal Article

Conventional dendritic cells are the critical donor APC presenting alloantigen after experimental bone marrow transplantation

Markey, KA, Banovic, T, Kuns, RD, Olver, SD, Don, ALJ, Raffelt, NC, Wilson, YA, Raggatt, LJ, Pettit, AR, Bromberg, JS, Hill, GR and MacDonald, KPA (2009). Conventional dendritic cells are the critical donor APC presenting alloantigen after experimental bone marrow transplantation. BLOOD, 113 (22), 5644-5649. doi: 10.1182/blood-2008-12-191833

Conventional dendritic cells are the critical donor APC presenting alloantigen after experimental bone marrow transplantation

2009

Conference Publication

Osteomacs: Osteoclast Precursors During Inflammatory Bone Disease but Regulators of Physiologic Bone Remodeling

Raggatt, L., Chang, M., Alexander, K., Maylin, E., Walsh, N., Gravallese, E., Hume, D. and Pettit, A. (2009). Osteomacs: Osteoclast Precursors During Inflammatory Bone Disease but Regulators of Physiologic Bone Remodeling. Australian Society of Bone and Mineral Research (ASBMR) 31st Annual Meeting, Denver, CO, United States, 11-15 September, 2009. United States: American Society for Bone and Mineral Research.

Osteomacs: Osteoclast Precursors During Inflammatory Bone Disease but Regulators of Physiologic Bone Remodeling

2009

Conference Publication

Osteomacs are critical for optimal intramembranous bone formation in a tibial defect model of bone healing

Alexander, K. A., Raggatt, L. J., Chang, M. K., Maylin, E. R., Muller, R., Kohler, T., Wu, A. C. K., Hume, D. A. and Pettit, A. R. (2009). Osteomacs are critical for optimal intramembranous bone formation in a tibial defect model of bone healing. 2nd Joint Meeting of the International Bone & Mineral Society and the Australian & New Zealand Bone & Mineral Society, Sydney, NSW, Australia, 21-25 March 2009. United States: Elsevier. doi: 10.1016/j.bone.2009.01.076

Osteomacs are critical for optimal intramembranous bone formation in a tibial defect model of bone healing

2009

Conference Publication

Osteomacs maintain the endosteal hematopoietic stem cell niche and participate in mobilization

Pettit, A. R., Sims, N. A., Winkler, I. G., Alexander, K. A., Helwani, F., Raggatt, L. J. and Levesque, J. P. (2009). Osteomacs maintain the endosteal hematopoietic stem cell niche and participate in mobilization. 2nd Joint Meeting of the International Bone and Mineral Society/Australian New Zealand Bone and Mineral Society, Sydney, Australia, 21-25 March, 2009. United States: Elsevier Inc.. doi: 10.1016/j.bone.2009.01.082

Osteomacs maintain the endosteal hematopoietic stem cell niche and participate in mobilization

2009

Conference Publication

Endosteal Macrophages Maintain the Hematopoietic Stem Cell (Hsc) Niche and Participate in Hsc Mobilization Induced by G-Csf or Chemotherapy

Levesque, J. P., Raggatt, L. J., Pettit, A. R., Sims, N. A., Bendall, L. J. and Helwani, F. (2009). Endosteal Macrophages Maintain the Hematopoietic Stem Cell (Hsc) Niche and Participate in Hsc Mobilization Induced by G-Csf or Chemotherapy. 38th Annual Scientific Meeting of the ISEH Society for Hematology and Stem Cells, Athens, Greece, 9-12 September 2009. NEW YORK: ELSEVIER SCIENCE INC.

Endosteal Macrophages Maintain the Hematopoietic Stem Cell (Hsc) Niche and Participate in Hsc Mobilization Induced by G-Csf or Chemotherapy

2009

Conference Publication

Osteomacs are Critical for Optimal Intramembranous Bone Formation in a Tibial Defect Model of Bone Healing

Alexander, K. A., Raggatt, L., Chang, M., Maylin, E., Muller, R., Kohler, T., Wu, A., Hume, D. and Pettit, A. (2009). Osteomacs are Critical for Optimal Intramembranous Bone Formation in a Tibial Defect Model of Bone Healing. Australian Society of Bone and Mineral Research (ASBMR) 31st Annual Meeting, Denver, Colorado, USA, 11-15 September, 2009. United States: American Society for Bone and Mineral Research.

Osteomacs are Critical for Optimal Intramembranous Bone Formation in a Tibial Defect Model of Bone Healing

2009

Conference Publication

Osteomacs: osteoclast precursors during inflammatory bone disease but regulators of physiologic bone remodelling

Raggatt, L. J., Chang, M. K., Alexander, K. A., Maylin, E. R., Walsh, N. C., Gravallese, E. M., Hume, D. A. and Pettit, A. R. (2009). Osteomacs: osteoclast precursors during inflammatory bone disease but regulators of physiologic bone remodelling. 2nd Joint Meeting of the International Bone & Mineral Society and the Australian & New Zealand Bone & Mineral Society, Sydney, Australia, 21-25 March, 2009. New York: Elsevier Science. doi: 10.1016/j.bone.2009.01.300

Osteomacs: osteoclast precursors during inflammatory bone disease but regulators of physiologic bone remodelling

2009

Conference Publication

Conventional dendritic cells are the critical donor APC presenting alloantigen after BMT

Markey, K, Banovic, T, Kuns, R, Raffelt, N, Olver, S, Don, A, Wilson, Y, Pettit, A, Bromberg, J, Hill, G and MacDonald, K (2009). Conventional dendritic cells are the critical donor APC presenting alloantigen after BMT. 35th Annual Meeting of the European-Group-for-Blood-and-Marrow-Transplantation, Goteborg Sweden, Mar 29-Apr 01, 2009. LONDON: NATURE PUBLISHING GROUP.

Conventional dendritic cells are the critical donor APC presenting alloantigen after BMT

2008

Journal Article

Osteal macrophages: A new twist on coupling during bone dynamics

Pettit, A. R., Chang, M. K., Hume, D. A. and Raggatt, L. J. (2008). Osteal macrophages: A new twist on coupling during bone dynamics. Bone, 43 (6), 976-982. doi: 10.1016/j.bone.2008.08.128

Osteal macrophages: A new twist on coupling during bone dynamics

2008

Journal Article

Osteal tissue macrophages are intercalated throughout human and mouse bone lining tissues and regulate osteoblast function in vitro and In Vivo

Chang, Ming K., Raggatt, Liza-Jane, Alexander, Kylie A., Kuliwaba, Julia S., Fazzalari, Nicola L., Schroder, Kate, Maylin, Erin R., Ripoll, Vera M, Hume, David A. and Pettit, Allison R. (2008). Osteal tissue macrophages are intercalated throughout human and mouse bone lining tissues and regulate osteoblast function in vitro and In Vivo. The Journal of Immunology, 181 (2), 1232-1244. doi: 10.4049/jimmunol.181.2.1232

Osteal tissue macrophages are intercalated throughout human and mouse bone lining tissues and regulate osteoblast function in vitro and In Vivo

2008

Journal Article

Re: Structural and cellular differences between metaphyseal and diaphyseal periosteum in different-aged rats

Pettit, Allison R., Hume, David A. and Raggatt, Liza-Jane (2008). Re: Structural and cellular differences between metaphyseal and diaphyseal periosteum in different-aged rats. Bone, 42 (4), 825-825. doi: 10.1016/j.bone.2007.12.217

Re: Structural and cellular differences between metaphyseal and diaphyseal periosteum in different-aged rats

2008

Journal Article

Microphthalmia transcription factor regulates the expression of the novel osteoclast factor GPNMB

Ripoll, V. M, Meadows, N. A., Raggatt, L. J., Chang, M. K., Pettit, A. R., Cassady, A. I. and Hume, D. A. (2008). Microphthalmia transcription factor regulates the expression of the novel osteoclast factor GPNMB. Gene, 413 (1-2), 32-41. doi: 10.1016/j.gene.2008.01.014

Microphthalmia transcription factor regulates the expression of the novel osteoclast factor GPNMB

2008

Conference Publication

Primary murine osteoblast cultures contain macrophages that enhance osteoblast mineralisation

Chang, M. K., Pettit, A. R., Schroder, K., Ripoll, V. M., Alexander, K. A., Hume, D. A. and Raggatt, L. (2008). Primary murine osteoblast cultures contain macrophages that enhance osteoblast mineralisation. ECTS 35th European Symposium on Calcified Tissues, Barcelona, Spain, 24-28 May 2008. New York, NY, U.S.A.: Springer New York. doi: 10.1007/s00223-008-9118-5

Primary murine osteoblast cultures contain macrophages that enhance osteoblast mineralisation

2008

Conference Publication

Primary murine osteoblast cultures contain macrophages that enhance osteoblast mineralization

Alexander, K. A., Chang, M. K., Hume, D. A., Pettit, A. R., Raggatt, L., Ripoli, V. M. and Schroder, K. (2008). Primary murine osteoblast cultures contain macrophages that enhance osteoblast mineralization. 35th European Symposium on Calcified Tissues, Barcelona, Spain, 24-28 May 2008. New York, USA: Springer. doi: 10.1007/s00223-008-9118-5

Primary murine osteoblast cultures contain macrophages that enhance osteoblast mineralization

Funding

Current funding

  • 2024 - 2028
    Quantum triangulation for deep tissue imaging in NIR-II
    The University of Queensland in America, Inc
    Open grant
  • 2022 - 2025
    Increasing hematopoietic stem cell niches post transplantation through enhancing bone marrow macrophage resilience and regeneration mechanisms
    NHMRC IDEAS Grants
    Open grant

Past funding

  • 2018 - 2020
    Colony-stimulating factor 1 receptor tyrosine kinase, a new target to treat acute myeloid leukemia
    Cancer Council Queensland
    Open grant
  • 2018 - 2019
    Nuclear medicine suite for animals
    UQ Major Equipment and Infrastructure
    Open grant
  • 2018 - 2020
    Osteal macrophages as therapeutic targets for fracture repair
    NHMRC Project Grant
    Open grant
  • 2017 - 2020
    Characterisation of Bone and Bone Marrow Resident Tissue Macrophages
    ARC Future Fellowships
    Open grant
  • 2016
    ANZBMS Gap Fellowship
    Australian & New Zealand Bone & Mineral Society
    Open grant
  • 2016 - 2019
    Recipient bone marrow macrophages contribute to haematopoietic stem cell transplantation success
    NHMRC Project Grant
    Open grant
  • 2016 - 2018
    Why macrophages promote heterotopic ossifications following spinal cord injuries
    NHMRC Project Grant
    Open grant
  • 2015 - 2019
    Mechanisms and Treatments of Heterotopic Ossification following Spinal Cord Injuries
    United States Congressionally Directed Medical Research Programs - Spinal Cord Injury Research Program
    Open grant
  • 2015 - 2019
    IL-22 as a Suppressor of Pancreatic Beta-Cell Stress and a Treatment for Diabetes
    NHMRC Project Grant
    Open grant
  • 2015 - 2016
    Macrophages facilitate prostate cancer bone metastasis.
    Cancer Council Queensland
    Open grant
  • 2014
    Influence of macrophage activation phenotype on fracture repair
    Arthritis Foundation of Australia
    Open grant
  • 2014 - 2015
    The role of macrophages in facilitating hematopoietic stem cell engraftment and reconstitution
    Cancer Council Queensland
    Open grant
  • 2013 - 2016
    Role of bone marrow cells in leukemia progression and resistance to chemotherapy
    NHMRC Project Grant
    Open grant
  • 2012
    Multi-user in vivo and ex vivo tissue-level mechanical testing instrument for bone and stem cell research
    NHMRC Equipment Grant
    Open grant
  • 2011 - 2014
    Novel treatment approaches to prevent joint fusion in ankylosing spondylitis
    NHMRC Project Grant
    Open grant
  • 2010
    Multi-user small animal digital x-ray imaging machine for bone, cancer, inflammation and stem cell research
    UQ Major Equipment and Infrastructure
    Open grant
  • 2010 - 2013
    Preclinical optimisation of intrauterine transplantation of fetal mesenchymal stem cells for osteogenesis imperfecta.
    NHMRC Project Grant
    Open grant
  • 2010 - 2013
    Regulation of Bone Dynamics by Osteal Tissue Macrophages (Osteomacs)
    NHMRC Project Grant
    Open grant
  • 2009 - 2011
    Towards selective targeting of HDACs for anti-inflammatory applications
    NHMRC Project Grant
    Open grant
  • 2008 - 2012
    NHMRC Career Development Award (Biomedical - Level 1): Osteal macrophages: novel regulators of osteoblast function and the endosteal stem cell niche
    NHMRC Career Development Award
    Open grant
  • 2007 - 2009
    Role of bone-associated macrophages in bone remodelling and bone disease
    NHMRC Project Grant
    Open grant
  • 2006
    Characterization of the role of T cell subsets in pathologic bone destruction
    Ramaciotti Foundation
    Open grant
  • 2006
    Role of macrophage migration inhibitory factor (MIF) in osteoclastogenesis and bone erosion in rheumatoid arthritis
    Arthritis Foundation of Australia
    Open grant
  • 2005
    Role of Macrophages Residing on the Bone Surface in Bone Remodelling and Repair
    UQ Early Career Researcher
    Open grant
  • 2001 - 2005
    NHMRC CJ Martin Fellowship: The role of T cell expression of receptor-activator of NFkB ligand (RANKL) in the pathogenesis of rheumatoid arthritis bone erosion
    NHMRC Training (Postdoctoral) Fellowship
    Open grant

Supervision

Availability

Professor Allison Pettit is:
Available for supervision

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Available projects

  • Deconvoluting Tissue Resident Macrophage Biology

    Project only open to Australian Domestic Applicants at this time with competitive stipend on offer.

    Analysis of single cell preparations from tissues is a mainstay of biological discovery research. Particularly in the current era of costly investment in increasingly high dimensional analysis of single cell samples toward generation of publicly available data sets. The team exposed an unrecognised technical phenomenon that has high potential to substantively compromise single cell data accuracy across a broad range of research fields including immunology and haematology. Specifically, tissue resident macrophages are fragmented during haematopoietic single cell suspension preparation and leave behind encapsulated remnants containing membrane and cytoplasmic molecules attached to other cells they were interacting with in situ. This phenomenon profoundly compromises accurate analysis of the data generated. Using this unique perspective, the project aims to 1) expose how widespread this phenomenon is in a diverse range of tissues across age; 2) develop optimised approaches to eliminate macrophage fragmentation during haematopoietic tissue single cell preparation; and 3) take advantage of this technical phenomenon to achieve a substantive knowledge gain in understanding bone marrow macrophage specialisation.

    The outcome of this research is a broad spectrum increase in the fidelity of biology research that utilises this common approach. This will elevate translatability of research outcomes and ultimately public confidence in the Australian biology research sector. It will create opportunity to collaborate with industry toward improved development of relevant reagents and instrument technology and inform development of digital tools to deconvolute this phenomenon when analysing big data sets.

Supervision history

Current supervision

Completed supervision

Media

Enquiries

Contact Professor Allison Pettit directly for media enquiries about:

  • Bone Marrow Transplantation
  • Osteoporosis Fragility Fracture
  • Tissue regeneration

Need help?

For help with finding experts, story ideas and media enquiries, contact our Media team:

communications@uq.edu.au