Contact
matt.brown“at”uq.edu.au
Ph. 07 3240 2870

Professor Matt Brown

Biography
Professor Matt Brown is Professor of Immunogenetics at the University of Queensland, based at the Diamantina Institute and Institute of Molecular Biosciences, a position he has held since September 2005. Prior to that he was Professor of Musculoskeletal Sciences, University of Oxford, where he worked since 1994. He initially trained in rheumatology in Sydney, and remains clinically active, with a special interest in ankylosing spondylitis (AS).

Research Interests
Professor Brown's group researches genetics of common diseases, particularly musculoskeletal diseases. They are the central genetics research centre for the Australo-Anglo-American Spondyloarthritis Consortium, the main international AS genetics group. In addition, the group are performing genomewide association studies in multiple sclerosis, osteoporosis and cervical cancer, and have genetics projects ongoing in rheumatoid arthritis and several other diseases. Professor Brown is a Principal Investigator of the Wellcome Trust Case-Control Consortium which did much of the development work and proof of principle studies for genomewide association studies, and is now involved in developing the approaches required for downstream genetics research (resequencing, fine-mapping, copy number variation studies). Professor Brown’s group also collaborate with researchers at the MRC Mammalian Research Facility Harwell, England, in ENU-mutagenesis approaches to develop new mouse strains with bone and joint disorders.

Selected Publications
1. Wellcome Trust Case-Control Consortium (Brown MA, principal investigator), Australo-Anglo-American Spondyloarthritis Consortium (Brown MA, principal investigator) (2007) “Association scan of 14,500 nonsynonymous SNPs in four diseases identifies autoimmunity variants”. Nat Genet, 39, 1329-1337.
2. Wellcome Trust Case-Control Consortium (Brown MA, principal investigator) (2007) “Genomewide association study of 14,000 cases in seven common diseases and 3,000 shared controls”. Nature. 447, 661-84.
3. Shore EM, Xu M, Feldman GJ, Fenstermacher DA, The FOP International Research Consortium, Brown MA and Kaplan FS. (2006) “A recurrent mutation in the BMP type 1 receptor ACVR1 causes inherited and sporadic fibrodysplasia ossificans progressiva”. Nature Genet, 38 (5), 525-527.
4. Zhang Y, Johnson K, Russell RGR, Wordsworth BP, Carr AJ, Terkeltaub RA and Brown MA (2005) “Association of “Sporadic” chondrocalcinosis with a -4bp G to A transition in the 5’-untranslated region of ANKH that promotes enhanced ANKH expression and extracellular PPi excess”. Arthritis Rheum. 52(4), 1110-7.
5. Timms AE, Crane AM,, Sims AM, Cordell HJ, Bradbury LA, Abbott A, Coyne MRE, Beynon O, Wallbank I, Duff GW, Calin A, Cardon LR, Wordsworth BP and Brown MA. (2004) “The interleukin 1 gene cluster contains a major susceptibility locus for ankylosing spondylitis”. Am J Hum Genet. 75, 587-95.
6. Williams CJ, Zhang Y, Timms A, Bonavita, G, Caeiro F. Broxholme J, Cuthbertson, J, Jones Y, Marchegiani R, Reginato R, Russell RGG, Wordsworth BP, Carr AJ and Brown MA.(2002) “Autosomal Dominant Familial Calcium Pyrophosphate Dihydrate Deposition Disease (CPPDD) Is Caused by Mutation in the Transmembrane Protein ANKH”. Am J Hum Genet. 71(4), 985-91.
7. Laval SH, Timms A, Edwards S, Bradbury L, Brophy S, Milicic A, Rubin L, Siminovitch KA, Weeks DE, Calin A, Wordsworth BP and Brown MA. (2001) “Whole-Genome Screening in Ankylosing Spondylitis: Evidence of Non-MHC Genetic-Susceptibility Loci”. Am J Hum Genet. 68(4), 918-926.
8. Koay MA, Woon PY, Miles L, Zhang Y, Duncan EL, Ralston SH, Compston JE, Cooper C, Keen R, Langdahl BL, MacLelland A, O’Riordan J, Pols H, Reid DM, Uitterlinden AG, Wass JAH and Brown MA. (2004) “Influence of LRP5 polymorphisms on normal variation in BMD”. J Bone Miner Res. 19, 1619-27.
9. Newton JL, Harney SM, Timms AE, Sims AM, Rockett K, Darke C, Wordsworth BP, Kwiatkowski D and Brown MA. (2004) “Dissection of class III major histocompatibility complex haplotypes associated with rheumatoid arthritis”. Arthritis Rheum. 50(7), 2122-9.
10. Sims AM, Shephard N, Carter K, Doan T, Dowling A, Duncan EL, Eisman J, Jones G, Nicholson G, Prince R, Seeman E, Thomas G, Wass JA and Brown MA. (2008) “Genetic Analyses in a Sample of Individuals With High or Low Bone Density Demonstrates Association With Multiple Wnt Pathway Genes.” J Bone Miner Res. 23(4):499-506.

Contact
e.duncan“at”uq.edu.au
Ph. 07 3240 5646

Dr Emma Duncan

Biography
Dr Emma Duncan’s undergraduate degree was in medicine at the University of Sydney, where she gained first class honours. She trained as a consultant physician and endocrinologist, mainly at the Oxford Centre for Diabetes, Endocrinology and Metabolism, UK, returning to Australia in 2005. Since her return has established herself as a key opinion leader in bone disease in Australia, particularly osteoporosis.

Dr Duncan’s research training was at the Wellcome Trust Centre for Human Genetics in Oxford, UK, where she completed a PhD in the genetics of osteoporosis. Her PhD work became the basis for the largest international linkage project in osteoporosis (the FAMOS consortium). In 2005 she was awarded a UQ Postdoctoral Research Fellowship for Women and the Royal College of Physicians Kincaid-Smith fellowship, and took up a research position at the Diamantina Institute. She was awarded an NHMRC Career Development Award in 2008.

Research Interests
Dr Duncan’s main research interest remains the genetic control of bone mass. She is currently the chief postdoctoral scientist directing an international genome-wide association study into high and low bone mass, as well as investigating the genetics of high bone mass syndromes through conventional means and next-generation sequencing approaches. She also has a clinical research interest in bone disease and skeletal dysplasias such as osteogenesis imperfecta.

Selected Publications
1. EL Duncan, MA Brown, JS Sinsheimer, JI Bell, AJ Carr, BP Wordsworth, JAH Wass (1999) “Suggestive Linkage of the Parathyroid Receptor Type 1 to Osteoporosis.” J Bone Miner Res 14(12):1993 - 99.
2. EL Duncan, L Cardon, JS Sinsheimer, JAH Wass and MA Brown (2003) “Gender and Site Specificity of Inheritance of Bone Mineral Density.” J Bone Miner Res 18(6)1531-8.
3. MA Koay, PY Woon, L Miles, Y Zhang, EL Duncan et al. (2004) “Influence of LRP5 polymorphisms on normal variation in BMD.” J Bone Miner Res 19(10): 1619-1627.
4. SH Ralston , N Galwey, I Mackay, OM Albagha, L Cardon, JE Compston, C Cooper, EL Duncan, et al (2005) “Loci for regulation of bone mineral density in men and women identified by genome wide linkage scan: the FAMOS study.” Hum Mol Genet. 14(7):943-51.
5. JP Ioannidis, MY Ng, P Sham, E Zintzaras, CM Lewis, H Deng, MJ Econs, D Karasik, M Devoto, EL Duncan, et al. (2007) Meta-analysis of genome wide scans provides evidence for gender and site specific regulation of bone mass. J Bone Miner Res 22(2) 173-83
6. C Vilarino-Guell, LJ Miles, EL Duncan, et al (2007) ‘PTHR1 Polymorphisms Influence BMD Variation through Effects on the Growing Skeleton’, Calcif Tissue Int 81(4):270-8
7. A-M Sims, N Shephard, K Carter, T Doan, A Dowling, EL Duncan et al (2008) Genetic analyses in a sample of individuals with high or low BMD shows association with multiple Wnt pathway genes. J Bone Miner Res 23(4):499-506.
8. NJ Timpson, JH Tobias, JB Richards, N Soranzo, EL Duncan et al “Common variants in the region around Osterix are associated with bone mineral density and growth in childhood” Hum Mol Gen (in press).
9. Ralston SH, Uitterlinden AG, Brandi ML, et al (including FAMOS collaborator Duncan EL). Large-scale evidence for the effect of the COLIA1 Sp1 polymorphism on osteoporosis outcomes: the GENOMOS study. PLoS Med 2006;3(4):e90.
10. MA Brown, LG Kennedy, AJ MacGregor, C Darke, EL Duncan et al (1997) “Genetic Susceptibility to Ankylosing Spondylitis in Twins: the Role of Genes, HLA and the Environment” Arthritis Rheum 40(10): 1823-8.

Contact
di.director"at"uq.edu.au

PA- Linda Barter
l.barter"at"uq.edu.au
Ph. 07 3240 5954

Professor Ian Frazer

Biography
Professor Ian Frazer was trained as a renal physician and clinical immunologist in Edinburgh, Scotland before emigrating in 1980 to Melbourne, Australia to pursue studies in viral immunology and autoimmunity at the Walter and Eliza Hall Institute of Medical Research with Prof Ian Mackay. In 1985 he moved to Brisbane to take up a teaching post with the University of Queensland, and he now holds a personal chair as head of the Diamantina Institute.

Professor Frazer holds research funding from several Australian and US funding bodies. He is a director of a biotechnology start-up company, Coridon, with an interest in optimising and targeting polynucleotide vaccine protein expression. He is president of Cancer Council Australia, and advises the World Health Organisation and the Bill and Melissa Gates Foundation on papillomavirus vaccines. He won the 2005 CSIRO Eureka Prize for Leadership in Science and the Australian of the Year in 2006. He was also awarded the 2008 Prime Minister's Prize for Science and the 2008 Balzan Prize for Preventative Medicine. Professor Frazer teaches immunology to undergraduate and graduate students of the University.

For a more detailed biography of Professor Ian Frazer, click here.

Research Interests
Professor Frazer's current research interests include immunoregulation and immunotherapeutic vaccines for papillomavirus associated cancers.

Selected Publications
1. Frazer IH. (2004) “Prevention of cervical cancer through papillomavirus vaccination.” Nat Rev Immunol 4(1):46-54.
2. Frazer IH, Quinn M, Nicklin JL, Tan J, Perrin LC, Ng P, et al. (2004) “Phase 1 study of HPV16-specific immunotherapy with E6E7 fusion protein and ISCOMATRIX (TM) adjuvant in women with cervical intraepithelial neoplasia.” Vaccine 23(2):172-81.
3. Stewart TJ, Smyth MJ, Fernando GJP, Frazer IH and Leggatt GR. (2003) “Inhibition of early tumor growth requires J alpha 18-positive (natural killer T) cells.” Cancer Res 63(12):3058-60.
4. Yan MY, Peng J, Jabbar IA, Liu XS, Filgueira L, Frazer IH and Thomas R. (2004) “Despite differences between dendritic cells and Langerhans cells in the mechanism of papillomavirus-like particle antigen uptake, both cells cross-prime T cells.” Virology 324(2):297-310.
5. Zhao KN, Liu WJ, Frazer IH. (2003) “Codon usage bias and A+T content variation in human papillomavirus genomes.” Virus Res 98(2):95-104.

Contact
m.kendall“at”uq.edu.au
Ph. 07 3346 4203 

Professor Mark Kendall

Biography
Professor Kendall joined the University of Queensland from the University of Oxford, where he was Associate Director of the PowderJect Centre for Gene and Drug Delivery Research, University Research Lecturer (Engineering Science) and Lecturer (Magdalen College). He also has both research commercialisation and consultancy experience, working with companies in the areas of drug delivery devices and vaccines. He is currently based at the Australian Institute for Bioengineering and Nanotechnology (AIBN), and has a joint appointment with the Diamantina Institute and the Faculty of Health Sciences.

Research Interests
Professor Kendall and his team focuses on the delivery of biomolecules and stimuli to cells in skin (and other soft tissue) using physical methods – putting vaccines where they need to go to generate far better immune responses than the needle and syringe. The goal is novel delivery strategies for step-change improvements in the treatment and vaccination of key major diseases.

Selected Publications
1. Kendall MAF, Chong Y and Cock A. (2007) “The mechanical properties of the skin epidermis in relation to targeted gene and drug delivery.” Biomaterials. 28(33):4968-4977.
2. Kendall MAF. (2006) “Engineering of needle-free physical methods to target epidermal cells for DNA vaccination.” Vaccine 24(21):4651-4656.
3. Raju PA, McSloy N, Truong NK and Kendall MAF. (2006) “Assessment of epidermal cell viability by Near Infra-Red Multi-photon Microscopy following ballistic delivery of gold micro-particles.” Vaccine 24(21):4644-4647.
4. Kendall MAF, Mitchell TJ, Costigan G, Armitage M, Lenzo JC, Thomas JA, Von Gardnier C, Zosky GR, Turner DJ, Stumbles PA, Sly PD, Holt PG and Thomas WR. (2006) “Down regulation of IgE allergic responses in the lung by epidermal biolistic micro-particle delivery.” J Allergy Clin Immunol. 117(2):275-282.
5. Kendall MAF, Mitchell TJ and Wrighton-Smith P. (2004) “Intradermal ballistic delivery of micro-particles into excised human skin for drug and vaccine applications.” J Biomech. 37(11):1733–1741.
6. Kendall MAF, Rishworth S, Carter FV and Mitchell TJ. (2004) “The effects of relative humidity and ambient temperature on the ballistic delivery of micro-particles into excised porcine skin.” J Invest Dermatol.122(3):739-746.
7. Kendall MAF. (2002) “The delivery of particulate vaccines and drugs to human skin with a practical, hand-held Shock Tube-based system.” Shock Waves. 12(1):22-30.

Contact
g.leggatt"at"uq.edu.au
Ph. 07 3240 5281

Dr Graham Leggatt

Biography
Dr Leggatt was born and raised in Brisbane where he completed a Bachelor of Science with honours at The University of Queensland in 1989. He then undertook PhD studies on the immune response against parasitic worms (hydatid disease) at the Queensland Institute of Medical Research (QIMR), receiving his doctorate in 1993. Dr Leggatt then travelled overseas to the National Institutes of Health in Washington D.C. (USA) to begin a postdoctoral position studying killer T cell immune responses to the AIDS virus in animal models. After almost 4 years abroad in Dr Jay Berzofsky’s lab, he then returned to the Princess Alexandra hospital in Brisbane to continue studies on the role of killer cells in viral infection (and cancer) with Professor Ian Frazer. Dr Leggatt’s current focus is on how killer T cells are silenced by cancers in the skin.

Research Interests
CD8 T cell tolerance to skin antigens/ skin tumours; combined immunotherapy/chemotherapy of tumours; and CD8 T cell avidity.

Selected Publications
1. Alexander-Miller M, Leggatt GR. and Berzofsky JA. (1996) “Selective expansion of high- or low-avidity cytotoxic T lymphocytes and efficacy for adoptive immunotherapy.” PNAS. 93,4102-4107.
2. Stewart TJ, Smyth MJ, Fernando GJP, Frazer IH and Leggatt GR (2003) “Inhibition of early tumor growth requires J 18-positive (NKT) cells.” Cancer Research 63: 3058-3060.
3. Matsumoto K, Leggatt GR, Zhong J, Liu X, DeKluyver R, Peters T, Fernando GJP, Liem A, Lambert P and Frazer IH. (2004) “Impaired antigen presentation limits effectiveness of combined active/passive immunotherapy for epithelial tumours.” J. Natl. Cancer Inst. 96: 1611-1619.
4. Stewart T, Fernando GJP, Frazer IH and Leggatt, G.R. (2004) “Tumor susceptibility to innate and adaptive immunotherapy changes during tumor maturation.” Immunol. Cell Biol. 82: 455-461.
5. Gu W, Putral L, Hengst K, Minto K, Saunders N, Leggatt G and McMillan NAJ. (2006) “Inhibition of cervical cancer cell growth in vitro and in vivo with lentiviral-vector delivered short hairpin RNA targeting human papillomavirus E6 and E7 oncogenes.” Cancer Gene Therapy 13:1023-1032.
6. Liu XS, Leggatt GR, Fernando GJP, Zhong J, Thomas R and Frazer IH (2006) “Overcoming original antigenic sin to generate new CD8 T cell IFN-γ responses in an antigen experienced host.” J. Immun. 177:2873-2879.
7. Leggatt GR and Frazer IH (2007) „HPV Vaccines: The beginning of the end for cervical cancer.” Current Opin. Immunol. 19:232-238.
8. Narayan S, Choyce A, Fernando GJP and Leggatt GR (2007) “Secondary immunization with high dose, heterologous peptide leads to CD8 T cell populations with reduced functional avidity.” Eur. J. Immunol. 37:406-415.

Contact
r.steptoe"at"uq.edu.au
Ph. 07 3240 5393

Dr Ray Steptoe

Biography
Dr Ray Steptoe undertook undergraduate studies in Anatomy and Human Biology and postgraduate studies in Immunology at the University of Western Australia. After further research training at the Thomas E. Starzl Transplantation Institute in Pittsburgh, USA, he returned to Australia to pursue research in autoimmune diabetes at the Walter and Eliza Hall Institute of Medical Research. In 2004, he moved to Brisbane to take up a Research Fellowship at the Diamantina Institute.

Dr Steptoe is now a Senior Research Fellow in the Dendritic Cell Biology group and heads a team of researchers investigating how pathogenic immune responses can be turned off. Dr Steptoe is currently a recipient of an NH&MRC Career Development Award.

Research Interests
Dr Steptoe’s research interests are aimed at determining the cellular and molecular pathways that are important in determining the fate of T-cell activation. In particular, studies are directed at understanding how to terminate pathogenic T cell responses with the goal of developing new therapeutic approaches to prevent or treat autoimmune diseases.

Selected Publications
1. Kenna TJ, Thomas R and Steptoe RJ. (2008) “Steady-state dendritic cells expressing cognate antigen terminate memory CD8+ T-cell responses.” Blood. 111:2091-2100.
2. Steptoe RJ, Ritchie JR, Wilson NS, Villadangos JA, Lew AM and Harrison LC. (2007) “Cognate CD4+ help elicited by resting DC does not impair tolerance induction in CD8+ T cells.” Journal of Immunology. 178: 2094-2103.
3. Wilson NS, Behrens GMN, Lundie RJ, Smith CM, Waithman J, Young L, Forehan SP, Mount A, Steptoe RJ, Shortman KD, de Koning-Ward T, Belz GT, Carbone FR, Crabb BS, Heath WR and Villadangos JA. (2006) “Systemic activation of dendritic cells by TLR ligands or malaria infection impairs cross-presentation and anti-viral immunity.” Nature Immunology. 7:165-172.
4. O'Sullivan BJ, Thomas HE, Pai S, Santamaria P, Iwakura Y, Steptoe RJ, Kay TWH and Thomas R. (2006) “IL-1beta breaks tolerance through expansion of CD25+ effector T cells.” Journal of Immunology. 176:7278-7287.
5. Narendran P, Neale AM, Lee BH, Ngui K, Steptoe RJ, Morahan G, Madsen O, Dromey JA, Jensen KP and Harrison LC. (2006) “Proinsulin is encoded by an RNA splice variant in human blood myeloid cells.” Proceeding of the National Academy of Sciences USA. 103:16430-16435.
6. O’Keeffe M, Brodnicki TC, Fancke B, Vremec D, Morahan G, Maraskovsky E, Steptoe RJ, Harrison LC and Shortman K. (2005) “Flt-3 ligand administration overcomes a genetically determined dendritic cell deficiency in NOD mice and protects against diabetes development.” International Immunology. 17:307-314.
7. Steptoe RJ, Ritchie JM, Jones LK and Harrison LC. (2004) “Autoimmune diabetes is suppressed by transfer of proinsulin-encoding Gr-1+ myeloid progenitors that differentiate in vivo into resting dendritic cells.” Diabetes. 54:434-442.
8. Steptoe RJ, Ritchie JM and Harrison LC. (2003) “Transfer of hematopoietic stem cells encoding an autoantigen prevents autoimmune diabetes.” Journal of Clinical Investigation. 111:1365-1371.
9. Steptoe RJ, Ritchie JM and Harrison LC. (2002) “Increased generation of dendritic cells from myeloid progenitors in the non-obese diabetic mouse.” Journal of Immunology. 168:5032-5041.
10. Villadangos JA, Cardoso MA, Steptoe RJ, Pooley J and Shortman K. (2001) “MHC class II expression in dendritic cells is regulated independently of invariant chain degradation.” Immunity. 14:739-749.

Contact
gethin.thomas"at"uq.edu.au
Ph. 07 3240 2755

Dr Gethin Thomas

Biography
Dr Gethin Thomas undertook his undergraduate and PhD studies in the dept of Biology at the University of Birmingham in the UK graduating with a PhD in Bone Cell Biology in 1993. He then undertook post-doctoral studies at the University of California in San Diego studying bone proteins biochemistry for two years. Continuing his interest in the bone field, he then spent five years in the Bone and Mineral Research Program at the Garvan Institute studying the role of vitamin D in bone. Dr Thomas then spent five years with a biotechnology company in Montréal leading a project characterising novel bone genes which resulted in the identification and characterisation of two novel bone genes, Ostn and Bril, with Ostn being patented and targeted for drug development. In 2005, Dr Thomas returned to academia in Australia to work with Professor Matthew Brown in the Musculoskeletal Genetics Group, focusing on the functional characterisation of genes identified by genetic screens in bone and joint disease.

Research Interests
Since my PhD studies, I have studied the biology of the skeleton, specifically the process of bone formation and the cells controlling that process, the osteoblasts. My interests focus on the roles of specific genes in skeletal regulation and more recently on the identification and characterisation of novel genes involved in bone disease, in particular ankylosing spondylitis and osteoporosis. We hope that identification of novel genes and pathways controlling bone formation can lead to the development of new drugs to target the replacement of lost bone and halt the progress of degenerative skeletal conditions.

Selected Publications
1. Moffatt P, Gaumond MH, Salois P, Sellin K, Bessette MC, Godin E, Tambasco de Oliveira P, Atkins GJ, Nanci A and Thomas G (2008) “Bril, A Novel Bone-Specific Modulator of Mineralisation.” Journal of Bone and Mineral Research. 23:1497-1508.
2. Sims A, Shephard N, Carter K, Doan T, Dowling A, Eisman J, Duncan E, Jones G, Nicholson G, Prince R, Seeman E, Thomas G, Wass J and Brown M (2008) “Genetic analyses in a sample of individuals with high or low bone density demonstrates association with multiple Wnt pathway genes.” Journal of Bone and Mineral Research. 23:499-506.
3. Thomas G, Moffatt P, Sellin K, Bessette M-C, Lafreniere F, Akhouayri O, St-Arnaud R and Lanctot C (2007) “Osteocrin is a specific ligand of the natriuretic peptide clearance receptor that modulates bone growth.” Journal of Biological Chemistry. 282:36454-36462
4. Thomas GP, Baldock PA, Hodge JM, SUK Baker, U Dressel, O’Loughlin PD, Nicholson GC, Briffa KH, Eisman JA and Gardiner EM (2006) “Vitamin D action and regulation of bone remodelling: Suppression of osteoclastogenesis by the mature osteoblast.” Journal of Bone and Mineral Research. 21:1618-1626.
5. Thomas G, Moffatt P, Salois P, Gaumond M, Gingras R, Miao D, Goltzman D and Lanctot C (2003) “Osteocrin, a novel bone-specific secreted protein that modulates the osteoblast phenotype.” Journal of Biological Chemistry. 278:50563-50571.
6. Baldock PA, Sainsbury A, Couzens M, Thomas GP, Enriquez RF, Gardiner EM and Herzog H (2002) “Neuropeptide Y2 receptor has a role in bone homeostasis independent of body weight.” Journal of Clinical Investigation. 109:915-921.

Contact
ranjeny.thomas"at"uq.edu.au
Ph. 07 3240 5365

Professor Ranjeny Thomas

Biography
Professor Thomas is a graduate of the University of Western Australia. She received her MBBS in 1984, and then trained in Perth as a rheumatologist. She commenced a research fellowship with Peter Lipsky at Southwestern Medical Center, University of Texas in 1990, where she first identified and characterised human circulating dendritic cell precursors. For more than 10 years in studying the function of dendritic cells in autoimmune diseases, she has written many articles, including several hypothetical articles on the immuno-pathogenesis of rheumatoid arthritis. She was appointed as Senior Lecturer at The University of Queensland in 1994, and promoted to Professor in 2004. Ranjeny is founder and a director of the spin-off company, Dendright, which is developing vaccines to suppress autoimmune diseases.

Research Interests
Professor Thomas’ research is focused on the study of the biology and clinical use of human dendritic cells in autoimmune disease. It has explored basic mechanisms of immunity and dendritic cell function in autoimmune disease. This has given rise to several clinical applications, including:

• A antigen-specific vaccine to treat rheumatoid arthritis
• A therapeutic platform for antigen-specific immunotherapy
• A novel diagnostic test for identification of those at risk of type 1 (juvenile) diabetes
• Novel immunotherapy for type 1 diabetes
  Research projects span from understanding dendritic cell function through analysis of signalling pathways, in vivo studies of tolerance, through to clinical trials of tolerance in autoimmunity, and clinical studies of risk factors in rheumatoid arthritis and type 1 diabetes.

Selected Publications
1. Smithers M, O’Connell K, MacFadyen S, Chambers M, Greenwood K, Boyce A, Abdul-Jabbar I, Barker K, Grimmett K, Walpole E and R Thomas. (2003) “Clinical response after intradermal immature dendritic cell vaccination in metastatic melanoma is associated with immune response to particulate antigen.” Cancer Immunol Immunother. 52: 41-52.
2. Martin E, O’Sullivan BJ, Low P and R Thomas. (2003) “Antigen-specific suppression of a primed immune response by dendritic cells mediated by regulatory T cells secreting interleukin-10.” Immunity 18:155-67.
3. O’Sullivan BJ and R Thomas. (2003) “CD40 and dendritic cell function.” Crit Rev Immunol. 23:83-107.
4. Peng JC, Thomas R and LK Nielsen. (2005) “Generation and maturation of DC for clinical application under serum-free conditions.” J Immunother. 28:599-609.
5. Thomas R, and W Arend. (2005) “Dendritic cells, follicular dendritic cells and monocytes.” In Kelley WN, Harris ED, Ruddy MD and Sledge CB (eds) Textbook of Rheumatology 7th edition. W.B. Saunders Company, Philadelphia.
6. Cavanagh LL, Boyce A, Smith L, Padmanabha J, Filgueira L, Pietschmann P and R Thomas. (2005) “Rheumatoid arthritis synovium contains plasmacytoid dendritic cells.” Arthritis Res Ther 7:R230-R240.
7. Thomas R. (2005) “Viewpoint. The TRAF6-NFκB signaling pathway in autoimmunity: not just inflammation.” Arthritis Res Ther 7:170-173.
8. O’Sullivan BJ, Thomas HE, Pai S, Santamaria P, Iwakura Y, Steptoe RJ, Kay TWH and R Thomas. (2006) “IL-1 breaks tolerance through expansion of CD25+ effector T cells.” J Immunol 176: 7278-7287.
9. Hannawi S, Haluska B, Marwick TH and R Thomas. (2007) “Atherosclerotic disease is increased in recent onset rheumatoid arthritis: a critical role for inflammation.” Arthritis Res Ther 9:R116.
10. Mollah ZUA, Pai S, Moore C, O’Sullivan BJ, Harrison MJ, Peng J, Phillips K, Prins JB, Cardinal J and R Thomas. (2008) “Abnormal NF-κB function characterizes human type 1 diabetes dendritic cells and monocytes.” J Immunol 180:3166-75.