Dr Xiao-Qing Wei
Senior Lecturer in Immunology, School of Dentistry
- Email:
- weix1@cardiff.ac.uk
- Telephone:
- +44 29207 44529
Dr. Xiao-Qing Wei is a Senior Lecturer in Immunology. His research focuses on the study of cytokine function in infection and immunity. He is one of the pioneer researchers in the identification of IL-35 and its application as an immune suppressing molecule in rheumatoid arthritis. His work has significantly contributed to the understanding of the mechanism of autoimmune and inflammatory diseases.
Dr. Xiao-Qing Wei graduated in medicine from the Medical School of Peking University (Beijing Medical University) in Beijing, China, and worked in the Beijing Hepatitis Research Institute of Youan Hospital, where he carried out research on infectious diseases, particularly hepatitis. He joined an immunology group at the University of Glasgow to investigate the role of inducible nitric oxide (iNOS) in infection and immunity and gained a PhD at the University of Glasgow. His post-doctoral research has concentrated on investigating the role of some important cytokines such as IL-15, IL-18, IL-23 and IL-27 in T cell development. The primary aim of his research in infectious and autoimmune diseases is to develop a practical anti-cytokine therapy to treat the inflammatory disorder, such as rheumatoid arthritis (RA). As a Senior Research Fellow, his research was supported by Arthritis Research UK to study the function of IL-18 and its receptors in RA. During that time, Dr Wei applied his research to studying the mechanism of anti-inflammation. Dr Wei is a pioneer researcher in the discovery of IL-35 and demonstrated its immune suppressing role in the treatment of the joint inflammation in mouse collagen induced arthritis model, which closely mimics rheumatoid arthritis in humans. His IL-35 study contributed significantly to the understanding of inflammatory disease mechanisms and may also benefit in future therapies of human autoimmune and inflammatory disorders. He was first appointed as a Lecturer in School of Dentistry, Cardiff University and was recently promoted to Senior Lecturer. Dr Wei's current research now focuses on the study of the role of novel IL-34 and IL-35 cytokines in the regulation of host immunity, particular concerning tissue macrophages andCandida infection, tumour survival, skin vaccine and skin/spinal wound healing. He is also interested in studying the functions of cytokine associations with mineralised tissue destruction related to RA, osteoarthritis and periodontal diseases.
Honours and awards
MB BCh, Medical School of Peking University (Beijing Medical University)PhD, University of Glasgow
2019
- Williams, A.et al. 2019. Immunohistochemical expression patterns of inflammatory cells involved in Chronic Hyperplastic Candidosis. Pathogens 8(4), article number: 232. (10.3390/pathogens8040232)
- Wang, X.et al. 2019. A generic coordination assembly-enabled nanocoating of individual tumor cells for personalized immunotherapy. Advanced Healthcare Materials 8(17), article number: 1900474. (10.1002/adhm.201900474)
- Morse, D.et al. 2019. Molecular community profiling of the bacterial microbiota associated with denture-related stomatitis. Scientific Reports 9, article number: 10228. (10.1038/s41598-019-46494-0)
- Koshy, B.et al. 2019. Array analysis for T-cell associated cytokines in gingival crevicular fluid: Identifying altered profiles associated with periodontal disease status. Journal of Dentistry 85, pp. 39-46. (10.1016/j.jdent.2019.04.009)
- Morse, D.et al. 2019. Modulation of Candida albicans virulence in in vitro biofilms by oral bacteria. Letters in Applied Microbiology 68(4), pp. 337-343. (10.1111/lam.13145)
2018
- Morse, D.et al. 2018. Denture-associated biofilm infection in 3-dimensional 1 oral mucosal tissue models. Journal of Medical Microbiology 67(3), pp. 364-375. (10.1099/jmm.0.000677)
2017
- Shi, G.et al. 2017. Enhanced antitumor immunity by targeting dendritic cells with tumor cell lysate-loaded chitosan nanoparticles vaccine. Biomaterials 113, pp. 191-202. (10.1016/j.biomaterials.2016.10.047)
2016
- Li, P.et al. 2016. PLGA nano/micro particles encapsulated with pertussis toxoid (PTd) enhances Th1/Th17 immune response in a murine model. International Journal of Pharmaceutics 513(1-2), pp. 183-190. (10.1016/j.ijpharm.2016.08.059)
- Zhang, G.et al. 2016. The role of Kv1.2 channel in electrotaxis cell migration. Journal of Cellular Physiology 231(6), pp. 1375-1384. (10.1002/jcp.25259)
- Zhang, S.et al. 2016. Decreased interleukin-35 is associated with higher risk of pregnancy morbidity in patients with antiphospholipid syndrome. Clinical and Experimental Rheumatology 34(3), pp. PI 0562-PF 0563.
- Zhang, S. L.et al. 2016. Decreased interleukin-35 levels are associated with higher risk of pregnancy morbidity in patients with antiphospholipid syndrome. Clinical and Experimental Rheumatology 34(3), pp. 562-563.
- Song, B.et al. 2016. Bladder smooth muscle cells differentiation from dental pulp stem cells: future potential for bladder tissue engineering. Stem Cells International 2016, article number: 6979368. (10.1155/2016/6979368)
2015
- Eastwood, S. E.et al. 2015. Osteoclastogenesis-related cytokines and peri-prosthetic osteolysis in revision metal-on-metal total hip replacements. Hip International 25(4), pp. 355-360. (10.5301/hipint.5000241)
- Boros-Majewska, J.et al. 2015. A novel in vitro assay for assessing efficacy and toxicity of antifungals using human leukemic cells infected with Candida albicans. Journal of Applied Microbiology 119(1), pp. 177-187. (10.1111/jam.12817)
- Haan, N.et al. 2015. Crosstalk between macrophages and astrocytes affects proliferation, reactive phenotype and inflammatory response, suggesting a role during reactive gliosis following spinal cord injury. Journal of Neuroinflammation 12, article number: 109. (10.1186/s12974-015-0327-3)
- Liu, J.et al. 2015. Electric signals regulate directional migration of ventral midbrain derived dopaminergic neural progenitor cells via Wnt/GSK3β signaling. Experimental Neurology 263, pp. 113-121. (10.1016/j.expneurol.2014.09.014)
- Cavalcanti, Y. W.et al. 2015. Virulence and pathogenicity of Candida albicans is enhanced in biofilms containing oral bacteria. Biofouling 31(1), pp. 27-38. (10.1080/08927014.2014.996143)
- Xia, T.et al. 2015. Plasma Interleukin-37 is elevated in patients with rheumatoid arthritis: Its correlation with disease activity and Th1/Th2/Th17-related cytokines. Disease Markers 2015, article number: 795043. (10.1155/2015/795043)
- Xu, R.et al. 2015. IL-34 suppresses 'Candida albicans' induced TNFα production in M1 macrophages by downregulating expression of Dectin-1 and TLR2. Journal of Immunology Research 2015, article number: 328146. (10.1155/2015/328146)
2014
- Boros-Majewska, J.et al. 2014. Novel Nystatin A1 derivatives exhibiting low host cell toxicity and antifungal activity in an in vitro model of oral candidosis. Medical Microbiology and Immunology 203(5), pp. 341-355. (10.1007/s00430-014-0343-4)
- Alves, C. T.et al. 2014. Candida albicans promotes invasion and colonisation of Candida glabrata in a reconstituted human vaginal epithelium. Journal of Infection 69(4), pp. 396-407. (10.1016/j.jinf.2014.06.002)
2013
- Rogers, H.et al. 2013. Immune response and candidal colonisation in denture associated stomatitis. Journal of Clinical & Cellular Immunology 4(6), article number: 178. (10.4172/2155-9899.1000178)
- Williams, D. W.et al. 2013. Interactions of Candida albicans with host epithelial surfaces. Journal of Oral Microbiology 5, article number: 22434. (10.3402/jom.v5i0.22434)
- Zheng, X. F.et al. 2013. Lipopolysaccharide-induced M2 to M1 macrophage transformation for IL-12p70 production is blocked by Candida albicans mediated up-regulation of EBI3 expression. PLoS ONE 8(5), article number: e63967. (10.1371/journal.pone.0063967)
- Yang, J.et al. 2013. The prevention of restenosis in vivo with a VEGF gene and paclitaxel co-eluting stent. Biomaterials 34(6), pp. 1635-1643. (10.1016/j.biomaterials.2012.11.006)
- Long, J.et al. 2013. IL-35 over-expression increases apoptosis sensitivity and suppresses cell growth in human cancer cells. Biochemical and Biophysical Research Communications 430(1), pp. 364-369. (10.1016/j.bbrc.2012.11.004)
- Rogers, H.et al. 2013. Role of bacterial lipopolysaccharide in enhancing host immune response to Candida albicans. Clinical and Developmental Immunology 2013, article number: 320168. (10.1155/2013/320168)
2012
- Feng, G. J.et al. 2012. Conditional disruption of Axin1 leads to development of liver tumors in mice. Gastroenterology 143(6), pp. 1650-1659. (10.1053/j.gastro.2012.08.047)
- Do, D. V.et al. 2012. Interleukin-18 system plays an important role in keloid pathogenesis via epithelial-mesenchymal interactions. British Journal of Dermatology 166(6), pp. 1275-1288. (10.1111/j.1365-2133.2011.10721.x)
- Van Belle, T. L.et al. 2012. IL-15 augments TCR-Induced CD4+ T Cell Expansion In Vitro by Inhibiting the Suppressive Function of CD25High CD4+ T Cells. Plos One 7(9), article number: e45299. (10.1371/journal.pone.0045299)
2011
- Wei, X.et al. 2011. The Role of the IL-12 Cytokine Family in Directing T-Cell Responses in Oral Candidosis. Clinical & Developmental Immunology, article number: 697340. (10.1155/2011/697340)
2010
- Koutoulaki, A.et al. 2010. TNF alpha and TGF-beta 1 influence IL-18-induced IFN gamma production through regulation of IL-18 receptor and T-bet expression. Cytokine 49(2), pp. 177-184. (10.1016/j.cyto.2009.09.015)
2009
- Bo, H.et al. 2009. Elevated expression of transmembrane IL-15 in immune cells correlates with the development of murine lupus: A potential target for immunotherapy against SLE. Scandinavian Journal of Immunology 69(2), pp. 119-129. (10.111/j.1365.3083.2008.02197.x)
2008
- Chen, L.et al. 2008. IL-23 promotes osteoclast formation by up-regulation of receptor activator of NF-kappa B (RANK) expression in myeloid precursor cells. European Journal of Immunology 38(10), pp. 2845-2854. (10.1002/eji.200838192)
- Niedbala, W.et al. 2008. Interleukin 27 attenuates collagen-induced arthritis. Annals of the Rheumatic Diseases 67(10), pp. 1474-1479. (10.1136/ard.2007.083360)
- Antonopoulos, C.et al. 2008. IL-18 is a key proximal mediator of contact hypersensitivity and allergen-induced Langerhans cell migration in murine epidermis. Journal of Leukocyte Biology 83(2), pp. 361-367. (10.1189/jlb.0604352)
- Anderson, I. E.et al. 2008. Production and Utilization of Interleukin-15 in Malignant Catarrhal Fever. Journal of Comparative Pathology 138(2-3), pp. 131-144. (10.1016/j.jcpa.2008.01.002)
- Bryson, K. J., Wei, X. and Alexander, J. 2008. Interleukin-18 enhances a Th2 biased response and susceptibility to Leishmania mexicana in BALB/c mice. Microbes and Infection 10(7), pp. 834-839. (10.1016/j.micinf.2008.03.009)
- Phan, T. T.et al. 2008. Interleukin-18 system plays an important role in keloid pathogenesis via epithelial-mesenchymal interactions. Tissue Engineering Part A 14(5), pp. 749-749.
2007
- Niedbala, W.et al. 2007. IL-35 is a novel cytokine with therapeutic effects against collagen-induced arthritis through the expansion of regulatory T cells and suppression of Th17 cells [Erratum]. European Journal of Immunology 37(11), pp. 3293-3293.
- Niedbala, W.et al. 2007. IL-35 is a novel cytokine with therapeutic effects against collagen-induced arthritis through the expansion of regulatory T cells and suppression of Th17 cells. European Journal of Immunology 37(11), pp. 3021-3029. (10.1002/eji.200737810)
2006
- Mullen, A. B.et al. 2006. Endogenous interleukin-18 is involved in immunity to Leishmania donovani but its absence does not adversely influence the therapeutic activity of sodium stibogluconate. Immunology 119(3), pp. 348-354. (10.1111/j.1365-2567.2006.02438.x)
- Verri Jr, W. A.et al. 2006. IL-15 mediates immune inflammatory hypernociception by triggering a sequential release of IFN-γ, endothelin, and prostaglandin. Proceedings of the National Academy of Sciences 103(25), pp. 9721-9725. (10.1073/pnas.0603286103)
2005
- McInnes, I. B.et al. 2005. Septic arthritis in inducible NO synthase knockout mice. Arthritis and Rheumatism : Supplement 39(S9), pp. S115. (10.1002/art.1780391402)
2004
- Wei, X.et al. 2004. Host genetic background determines whether IL-18 deficiency results in increased susceptibility or resistance to murine Leishmania major infection. Immunology Letters 94(1-2), pp. 35-37. (10.1016/j.imlet.2004.04.001)
- Kerr, A. R.et al. 2004. Nitric oxide exerts distinct effects in local and systemic infections with Streptococcus pneumoniae. Microbial Pathogenesis 36(6), pp. 303-310. (10.1016/j.micpath.2004.02.001)
- Millington, O. R.et al. 2004. Interleukin-15 is not required for the induction or maintenance of orally induced peripheral tolerance. Immunology 113(3), pp. 304-309. (10.1111/j.1365-2567.2004.01965.x)
2003
- Liew, F. Y., Wei, X. and McInnes, I. B. 2003. Role of interleukin 18 in rheumatoid arthritis. Annals Of The Rheumatic Diseases 62, pp. 48-50. (10.1136/ard.62.suppl_2.ii48)
- Kuffova, L.et al. 2003. The effect of local and systemic administration of soluble IL-15 receptor alpha-chain in experimental corneal transplantation [Abstract]. Investigative Ophthalmology & Visual Science 44, pp. U620-U620.
- Komai-Koma, M.et al. 2003. Chemoattraction of human T cells by IL-18. The Journal of Immunology 170(2), pp. 1084-1090.
- Pollock, K. G. J.et al. 2003. Interleukin-18 plays a role in both the alum-induced T helper 2 response and the T helper 1 response induced by alum-adsorbed interleukin-12. Immunology 108(2), pp. 137-143. (10.1046/j.1365-2567.2003.01581.x)
- McInnes, I.et al. 2003. Innate response cytokines in inflammatory synovitis: novel targets and strategies. Arthritis Research & Therapy 5(S3), pp. 68-68. (10.1186/ar869)
2002
- Niedbala, W.et al. 2002. Nitric oxide preferentially induces type 1 T cell differentiation by selectively up-regulating IL-12 receptor beta 2 expression via cGMP. Proceedings of the National Academy of Sciences 99(25), pp. 16186-16191. (10.1073/pnas.252464599)
- Nguyen, K. B.et al. 2002. Coordinated and distinct roles for IFN-alpha beta, IL-12, and IL-15 regulation of NK cell responses to viral infection. The Journal of Immunology 169(8), pp. 4279-4287.
- Mulero, V.et al. 2002. Regulation of phagosomal iron release from murine macrophages by nitric oxide. Biochemical Journal 365(1), pp. 127-132.
- Khan, I. A.et al. 2002. Treatment with soluble interleukin-15 Ralpha exacerbates intracellular parasitic infection by blocking the development of memory CD8+T cell response. Journal of Experimental Medicine 195(11), pp. 1463-1470. (10.1084/jem.20011915)
- Nguyen, K. B.et al. 2002. Multiple signaling mechanisms for IFN-alpha/beta regulation of natural killer and memory CD8 T cell responses during viral infections.. Faseb Journal 16(4), pp. A287-A287.
- Canthaboo, C.et al. 2002. Investigation of role of nitric oxide in protection from Bordetella pertussis respiratory challenge. Infection and Immunity 70(2), pp. 679-684. (10.1128/IAI.70.2.679-684.2002)
- Niedbala, W., Wei, X. and Liew, F. Y. 2002. IL-15 induces type 1 and type 2 CD4(+) and CD8(+) T cells proliferation but is unable to drive cytokine production in the absence of TCR activation or IL-12/IL-4 simulation in vitro. European Journal of Immunology 32(2), pp. 341-347.
2001
- Armour, K. J.et al. 2001. Activation of the inducible nitric oxide synthase pathway contributes to inflammation-induced osteoporosis by suppressing bone formation and causing osteoblast apoptosis. Arthritis and Rheumatism 44(12), pp. 2790-2796. (10.1002/1529-0131(200112)44:12<2790::AID-ART466>3.0.CO;2-X)
- Esfandiari, E.et al. 2001. A proinflammatory role of IL-18 in the development of spontaneous autoimmune disease. The Journal of Immunology 167(9), pp. 5338-5347.
- Wei, X.et al. 2001. The sushi domain of soluble IL-15 receptor alpha is essential for binding IL-15 and inhibiting inflammatory and allogenic responses in vitro and in vivo. The Journal of Immunology 167(1), pp. 277-282.
- Wei, X.et al. 2001. Reduced incidence and severity of collagen-induced arthritis in mice lacking IL-18. The Journal of Immunology 166(1), pp. 517-521.
2000
- Leung, B. P.et al. 2000. Reduced incidence and severity of collagen-induced arthritis in mice lacking interleukin-18 (IL-18)[Abstract]. Arthritis and Rheumatism 43(S9), pp. S176-S176., article number: 657. (10.1002/art.1780432008)
- Smith, X. G.et al. 2000. Selective blockade of IL-15 by soluble IL-15 receptor alpha-chain enhances cardiac allograft survival. The Journal of Immunology 165(6), pp. 3444-3450.
- McInnes, I. B.et al. 2000. Interleukin 18: a pleiotropic participant in chronic inflammation. Immunology Today 21(7), pp. 312-315. (10.1016/S0167-5699(00)01648-0)
- van't Hof, R. J.et al. 2000. Requirement of the inducible nitric oxide synthase pathway for IL-1-induced osteoclastic bone resorption. Proceedings of the National Academy of Sciences of the United States of America 97(14), pp. 7993-7998. (10.1073/pnas.130511497)
- Leung, B. P.et al. 2000. Combined effects of IL-12 and IL-18 on the induction of collagen-induced arthritis. The Journal of Immunology 164(12), pp. 6495-6502.
- Feng, G. J.et al. 2000. Erk and p38 MAP kinases differentially regulate the lipopolysaccharide-mediated induction of inducible nitric oxide synthase and interleukin-12 in macrophages: Leishmania phosphoglycans subvert macrophage interleukin-12 production by targetting Erk MAP kinase. Presented at: 6th International Meeting on the Biology of Nitric Oxide, Stockholm, Sweden, 5-8 September 1999 Presented at Moncada, S. ed.The Biology of Nitric Oxide Part 7: Proceedings of the 6th International Meeting on the Biology of Nitric Oxide, held in Stockholm, Sweden, in September 1999. Portland Press Proceedings Vol. 16. London: Portland Press pp. 222.
- Lawrence, C. E.et al. 2000. Nitric oxide mediates intestinal pathology but not immune expulsion during Trichinella spiralis infection in mice. The Journal of Immunology 164(8), pp. 4229-4234.
- Duffield, J. S.et al. 2000. Activated macrophages direct apoptosis and suppress mitosis of mesangial cells. The Journal of Immunology 164(4), pp. 2110-2119.
1999
- Wei, X.et al. 1999. Altered immune responses and susceptibility to Leishmania major and Staphylococcus aureus infection in IL-18-deficient mice. The Journal of Immunology 163(5), pp. 2821-2828.
- McInnes, I. B.et al. 1999. Soluble interleukin-15 alpha chain administration during murine infectious arthritis defines a role for IL-15 in regulating T helper 1 responses.. Arthritis and Rheumatism 42(9), pp. S337-S337.
- Millar, A. E.et al. 1999. T-cell responses during Trypanosoma brucei infections in mice deficient in inducible nitric oxide synthase. Infection and Immunity 67(7), pp. 3334-3338.
- Niedbala, W.et al. 1999. Effects of nitric oxide on the induction and differentiation of Th1 cells. European Journal of Immunology 29(8), pp. 2498-2505. (10.1002/(SICI)1521-4141(199908)29:08<2498::AID-IMMU2498>3.0.CO;2-M)
- Feng, G.et al. 1999. Extracellular signal-related kinase (ERK) and p38 mitogen-activated protein (MAP) kinases differentially regulate the lipopolysaccharide-mediated induction of inducible nitric oxide synthase and IL-12 in macrophages: Leishmania phosphoglycans subvert macrophage IL-12 production by targeting ERK MAP kinase. The Journal of Immunology 163(12), pp. 6403-6412.
1998
- Ruchatz, H.et al. 1998. Soluble IL-15 receptor alpha-chain administration prevents murine collagen-induced arthritis: A role for IL-15 in development of antigen-induced immunopathology. The Journal of Immunology 160(11), pp. 5654-5660.
- Huang, F.et al. 1998. Mice defective in fas are highly susceptible to Leishmania major infection despite elevated IL-12 synthesis, strong Th1 responses, and enhanced nitric oxide production. The Journal of Immunology 160(9), pp. 4143-4147.
- Cattell, V.et al. 1998. Anti-GBM glomerulonephritis in mice lacking nitric oxide synthase type 2. Kidney International 53(4), pp. 932-936.
- MacLean, A.et al. 1998. Mice lacking inducible nitric-oxide synthase are more susceptible to herpes simplex virus infection despite enhanced Th1 cell responses. Journal of General Virology 79(4), pp. 825-830.
- Zaragoza, C.et al. 1998. The role of inducible nitric oxide synthase in the host response to Coxsackievirus myocarditis. Proceedings of the National Academy of Sciences of the United States of America 95(5), pp. 2469-2474.
- McInnes, I. B.et al. 1998. Septic arthritis following Staphylococcus aureus infection in mice lacking inducible nitric oxide synthase. The Journal of Immunology 160(1), pp. 308-315.
- Huang, F.et al. 1998. Nitric oxide regulates Th1 cell development through the inhibition of IL-12 synthesis by macrophages. European Journal of Immunology 28(12), pp. 4062-4070. (10.1002/(SICI)1521-4141(199812)28:12<4062::AID-IMMU4062>3.0.CO;2-K)
1997
- Liew, F. Y., Wei, X. and Proudfoot, L. 1997. Cytokines and nitric oxide as effector molecules against parasitic infections. Philosophical Transactions Of The Royal Society B-Biological Sciences 352(1359), pp. 1311-1315.
- Casey, J. J.et al. 1997. Skin allograft rejection in mice lacking inducible nitric oxide synthase. Transplantation 64(4), pp. 589-593. (10.1097/00007890-199708270-00007)
1996
- Casey, J. J.et al. 1996. Allograft rejection by mice lacking inducible nitric oxide synthase. Immunology 89, pp. ORI24-ORI24.
- Proudfoot, L.et al. 1996. Regulation of the expression of nitric oxide synthase and leishmanicidal activity by glycoconjugates of Leishmania lipophosphoglycan in murine macrophages. Proceedings Of The National Academy Of Sciences Of The United States Of America 93(20), pp. 10984-10989.
- McInnes, I. B.et al. 1996. Production of nitric oxide in the synovial membrane of rheumatoid and osteoarthritis patients. Journal Of Experimental Medicine 184(4), pp. 1519-1524.
- Baylis, S. A.et al. 1996. Expression of inducible nitric oxide synthase in the developing mouse placenta.. Biology Of Nitric Oxide, Pt 5 10, pp. 237-237.
1995
- Wei, X.et al. 1995. Altered immune responses in mice lacking inducible nitric oxide synthase [Letter]. Nature 375(6530), pp. 408-411. (10.1038/375408a0)
- Moss, D. W.et al. 1995. Enzymatic characterization of recombinant murine inducible nitric-oxide synthase. European Journal Of Pharmacology-Molecular Pharmacology Section 289(1), pp. 41-48. (10.1016/0922-4106(95)90166-3)
Apart from research undertaken at the School of Dentistry, Cardiff University, Dr. Wei also has responsibility for teaching on the oral ecosystem course for year 2 BDS students. He is involved in the examination and assessment of this course. Dr Wei also has an assessment role in Problem Based Learning (PBL). Recently, he has took a model lead role in the mentorship of year 2 students post presentation and assessment. Dr Wei also supervises projects of final year BDS students. ed on )
Research interests
Cytokines play a pivotal role in controlling the outcome of infectious and inflammatory diseases by regulation of host innate and adaptive immunity. My research has focused on the understanding of the role of some important pro-inflammatory cytokines, such as IL-15, IL-18, IL-12, IL-23, IL-27 and the novel anti-inflammatory cytokines, IL-34 and IL-35, in disease processes in order to find practical ways to regulate host immune responses for treatment. Inflammatory cytokines promote host immunity against pathogen invasion and tumour formation. However, over reaction also results in autoimmune and inflammatory diseases, such as rheumatoid arthritis and periodontal diseases. Host cells produce anti-inflammatory cytokines to avoid this over-reaction. One of these important anti-inflammatory cytokines is IL-35. I am one of the pioneer researchers who discovered IL-35 and identified its anti-inflammatory role using a mouse rheumatoid arthritis model. My research is continuing to understand the role of IL-35 in other human diseases such as candidosis, tumour development and neuronal degeneration. Through understanding the biological mechanisms of IL-35 in human diseases, development of therapies to treat those human diseases may be achieved.
Tissue resident macrophages occupy 5-10% of the cell component of tissues and play important roles in the removal of dead cells and cytokine production during disease processes. Tissue macrophages are highly heterogeneous and exhibit plasticity. Inflammatory tissues with higher pro-inflammatory cytokines will induce macrophages to their M1 phenotype, while in an anti-inflammatory environment with higher levels of growth factors and anti-inflammatory cytokines, conversion to the M2 phenotype is favoured. My research aims to determine how the tissue environment modulates this macrophage phenotype transition and how these macrophages contribute to the outcome of human diseases, including candidosis, tumour development, neuron degeneration and tissue repair.Vaccines are effective tools in preparing the host immune system for protection against pathogen invasion. Cytokines also play a key role during vaccination. T cell development in a certain cytokine environment determines the types of immunity,i.e.cellular or humoral immunity. Many failures of vaccination result from the stimulation of the wrong type immune responses. Cell mediated immunity is absolutely critical for the success of some vaccination. Currently I am working on developing a vaccination process that combines cytokines with physical stimulation, nanoparticle and microneedle delivery system. The novel protocol and device for vaccination should be highly benefitial in promoting human health.
Current Projects
Development of a novel electric-field mediated PLGA micro-needle vaccine patch
Studying the role of novel cytokines, IL-34 and IL-35, in the regulation of host immune response against tumour and yeast infection. Studying the influential role of IL-12 family cytokines in dopaminegic neuronal cell death in Parkinson's disease
Studying the influential role of IL-12 family cytokines in dopaminegic neuronal cell death in Parkinson's disease