My lab research is focused on molecular analysis of inflammatory and autoimmune diseases. We apply ‘omics’ technologies, including transcriptomics and proteomics to the study of human inflammatory disease, in order to develop targetted therapeutics.
Our primary focus has been on rheumatoid arthritis (RA), but we’ve found that experimental systems and techniques used to study RA are relevant to many other inflammatory diseases, and we now have active research programs in vasculitis, myositis and lupus. We also have a strong interest in developing therapeutic antibodies and several of these have gone into clinical trials. In addition to engineered antibodies, we have formed a collaboration with Australian Red Cross Lifeblood to study the naturally occurring human antibody repertoire in hemolytic disease of the newborn.
A major research theme of my lab is to investigate how the cytokines G-CSF and GM-CSF promote inflammatory diseases. This has led to collaborations with the biotechnology sector (CSL, MedImmune and Kiniksa) and the development of antibody-based therapies to the G- and GM-CSF receptors that are currently in clinical trials.
Australia, The University of Melbourne, PhD 1993
Australia, The University of Sydney, MB BS 1981
University of Melbourne
2007 Parr Prize for Research, Australian Rheumatology Association
2016 Fellow, Australian Academy of Health and Medical Sciences
1996 – Current Research support, John T Reid Charitable Trusts
2004-2022 Project, Development and Program grants, National Health and Medical Research Council
2002-2022 Practitioner fellowships, National Health and Medical Research Council and MRFF
Project grants – Arthritis Foundation of Australia, Walkom Trust, Rebecca Cooper Medical Research Foundation, Ophthalmology Research Institute of Australia, National Heart Foundation, H & L Hecht Trust, Woodend Foundation, Beischer Foundation
1998-2021 Professor/Director, Rheumatology Unit, Royal Melbourne Hospital and University of Melbourne
GM-CSF primes cardiac inflammation in a mouse model of Kawasaki disease.
Stock AT, Hansen JA, Sleeman MA, McKenzie BS, Wicks IP. J Exp Med 2016
Targeting GM-CSF in inflammatory diseases. Wicks IP & Roberts AW. Nature Reviews Rheumatology 2016
A cytotoxic anti-IL3R a antibody targets key cells and alters cytokines implicated in systemic lupus erythematosus. Shereen Oon, Huy Huynh, Tsin Yee Tai, Milica Ng, Katherine Monaghan, Mark Biondo, Gino Vairo, Eugene Maraskovsky, Andrew D. Nash, Ian P Wicks*, Nicholas J. Wilson*. JCI Insight 2016 *co-senior authors
Dysregulated IL-1β-GM-CSF Axis in Acute Rheumatic Fever That Is Limited by Hydroxychloroquine. Kim ML, Martin WJ, Minigo G, Keeble JL, Garnham AL, Pacini G, Smyth GK, Speed TP, Carapetis J, Wicks IP. Circulation. 2018
Therapeutic Effects of a TANK-Binding Kinase 1 Inhibitor in Germinal Center-Driven Collagen-Induced Arthritis. Louis C, NgoD, D’Silva DB, Hansen J, Phillipson L, Jousset H, Novello P, Segal D, Lawlor KE, Burns CJ, Wicks IP. Arthritis Rheumatol. 2019
NK cell-derived GM-CSF potentiates murine autoantibody-induced inflammatory arthritis and is negatively regulated by CIS. Louis C, Guimaraes FSF, Yang Y, D’Silva DB, Kratina T, Dagley LF, Hediyeh-zadeh S, Rautela J, Davis MJ, Babon JJ, Ciric B, Vivier E, Alexander WS, Huntington ND*, Wicks IP*. J Exp Med. 2020. *co-senior authors
Efficacy and safety of mavrilimumab in giant cell arteritis: a phase 2, randomised, double-blind, placebo-controlled trial. Maria C Cid, Sebastian H Unizony, Daniel Blockmans, Elisabeth Brouwer, Lorenzo Dagna, Bhaskar Dasgupta, Bernhard Hellmich, Eamonn Molloy, Carlo Salvarani, Bruce C Trapnell, Kenneth J Warrington, Ian Wicks, Manoj Samant, Teresa Zhou, Lara Pupim, John F Paolini. Ann Rheum Dis 2022
mTOR inhibition prevents coronary artery remodeling in a murine model of Kawasaki disease. Angus. T. Stock, Sarah Parsons, Damian. B. D’Silva, Jacinta. A. Hansen, Varun. J. Sharma, Fiona James, Graham Starkey, Rohit D’Costa, Claire. L. Gordon & Ian. P. Wicks. Arth Rheum 2022
Targeting necroptosis in muscle fibers ameliorates inflammatory myopathies. Mari Kamiya, Fumitaka Mizoguchi, Kimito Kawahata, Dengli Wang, Masahiro Nishibori, Jessica Day, Cynthia Louis, Ian Wicks, Hitoshi Kohsaka, and Shinsuke Yasuda. Nature Communications 2022
CD98 controls the metabolic flexibility of low-density neutrophils mobilized by granulocyte colony stimulating factor. Katherine R Martin, Jessica A Day, Jacinta A Hansen, Damian B D’Silva, Huon L Wong, Peter Hickey, Alexandra Garnham, Daniela Zalcenstein, Belinda Lee, Tracey Baldwin, Shalin H. Naik, Pradeep Rajasekhar, Jarrod J Sandow, Brunda Nijagal, Tracy L. Putoczki, Nick Wilson, Ian P. Wicks. Clinical and Translational Medicine 2023
Rheumatoid arthritis (RA) is a common human inflammatory disease that targets synovial joints, causing chronic joint pain and leading to joint damage and progressive disability. The cause of RA remains unclear, although activation of innate and adaptive immune systems and increased production of cytokines are prominent features of RA. We aim to understand the biology of key effector cells and dysregulation of cytokine production and cytokine signalling in RA, in order to identify new therapeutic targets and biomarkers to more effectively treat RA. We have established a wide range of experimental systems to study RA, employing WEHI’s advanced technologies. In conjunction with the Centre for Biologic Therapies, we are developing several therapeutic antibodies to new targets.
Team members: Dr Cynthia Louis (email@example.com)
Kawasaki Disease (KD) causes cardiac vasculitis in children. Temporal arteritis (also called giant cell arteritis, GCA) is a similar condition in older adults. We have established an experimental model of KD and have been determining which cells and cytokines are the most suitable candidates for therapeutic intervention. We showed that GM-CSF is a critical cytokine in KD. Based on this and other research, an anti-GM-CSF receptor antibody has undergone clinical trials in GCA. We have also recently identified the mTOR pathway and its inhibitor rapamycin as another important pathway in KD.
Team members: Dr Angus Stock (firstname.lastname@example.org)
Myositis comprises a spectrum of poorly understood inflammatory diseases involving muscles. This is a new area of research for the Lab, employing in vitro and in vivo experimental models and advanced technologies, including spatial transcriptomics applied to human muscle biopsies.
Lab members: Dr Jess Day (email@example.com)
Rhesus D incompatability between mother and baby is a well recognised cause of HDN. remarkably, it can be largely prevented by administration of pooled anti-RhD immunoglobulins during pregnancy, derived from blood donors. As part of our Lab’s interests in therapeutic antibodies, we are collaborating with Australian Red Cross Lifeblood to fully characterise these naturally occurring anti-RhD antibodies.
Team member: Dr Behnaz Heydarchi (firstname.lastname@example.org)