Dr Xiao-Qing Wei

Uwch-ddarlithydd mewn Imiwnoleg, Ysgol Deintyddiaeth

: Ar gael fel goruchwyliwr ôl-raddedig

Mae Dr. Xiao-Qing Wei yn Uwch Ddarlithydd mewn Imiwnoleg. Mae ei ymchwil yn canolbwyntio ar astudio swyddogaeth cytokine mewn heintiau ac imiwnedd. Mae'n un o'r ymchwilwyr arloesol wrth adnabod IL-35 a'i gymhwyso fel moleciwl atal imiwnedd mewn arthritis gwynegol. Mae ei waith wedi cyfrannu'n sylweddol at ddealltwriaeth o fecanwaith clefydau hunanimiwn ac ymfflamychol.

2018

Morse, D., Wilson, M., Wei, X., Lewis, M. A. O., Bradshaw, D. J., Murdoch, C. and Williams, D. 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., Edmundson, M., Telezhkin, V., Gu, Y., Wei, X., Kemp, P. J. and Song, B. 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. L., Liu, N., Wei, X., Lu, Q., Mu, R. and Li, Z. G. 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.
Zhang, S., Liu, N., Wei, X., Lu, Q., Mu, R. and Li, Z. 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.
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

Boros-Majewska, J., Turczyk, L., Wei, X., Milewski, S. and Williams, D. W. 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)
Eastwood, S. E., John, A., Jones, S. A., Hodgson, H., Mason, D. J., Waddington, R. and Wei, X. 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)
Haan, N., Zhu, B., Wang, J., Wei, X. and Song, B. 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)
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)
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)
Xu, R., Sun, H., Williams, D. W., Jones, A. V., Al-Hussaini, A., Song, B. and Wei, X. 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)
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)

2014

Alves, C. T., Wei, X., Silva, S., Azeredo, J., Henriques, M. and Williams, D. W. 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)
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)

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., Jordan, R. P. C., Wei, X., Alves, C. T., Wise, M. P., Wilson, M. J. and Lewis, M. A. O. 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)
Rogers, H., Williams, D. W., Feng, G. J., Lewis, M. A. O. and Wei, X. 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)
Long, J., Zhang, X., Wen, M., Kong, Q., Lv, Z., An, Y. and Wei, X. 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)

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., Dooms, H., Boonefaes, T., Wei, X., Leclercq, G. and Grooten, J. 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., Rogers, H., Lewis, M. A. O. and Williams, D. W. 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., Langley, M. S., Sloan, A. J., Aeschlimann, D. and Wei, X. 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., Wei, X., Evans, B. A. J., Jiang, W. G. and Aeschlimann, D. 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., Cai, B., Wei, X., Patakas, A., Leung, B. P., McInnes, I. B. and Liew, F. Y. 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)
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.
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)
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)

2007

Niedbala, W., Wei, X., Cai, B., Hueber, A. J., Leung, B. P., McInnes, I. and Liew, F. Y. 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)
Niedbala, W., Wei, X., Cai, B., Hueber, A. J., Leung, B. P., McInnes, I. and Liew, F. Y. 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.

2006

Mullen, A. B., Lawrence, C. E., McFarlane, E., Wei, X. and Carter, K. C. 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., Cunha, T. M., Parada, C. A., Wei, X., Ferreira, S. H., Liew, F. Y. and Cunha, F. Q. 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., Gemmell, C. G., Wei, X. and Liew, F. Y. 2005. Septic arthritis in inducible NO synthase knockout mice. Arthritis and Rheumatism : Supplement 39(S9), pp. S115. (10.1002/art.1780391402)

2004

Wei, X., Niedbala, W., Xu, D., Luo, Z., Pollock, K. G. J. and Brewer, J. M. 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., Wei, X., Andrew, P. W. and Mitchell, T. J. 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., Wei, X., Garside, P. and Mowat, A. M. C. . 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., Taylor, J. A., Duncan, L., Liew, F. Y., Wei, X. and Forrester, J. V. 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., Gracie, J. A., Wei, X., Xu, D., Thomson, N., McInnes, I. B. and Liew, F. Y. 2003. Chemoattraction of human T cells by IL-18. The Journal of Immunology 170(2), pp. 1084-1090.
Pollock, K. G. J., Conacher, M., Wei, X., Alexander, J. and Brewer, J. M. 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., Leung, B. P., Gracie, J. A. G., Xu, D., Wei, X., Brewer, J. and Liew, F. Y. 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., Wei, X., Campbell, C., Thomson, D., Komai-Koma, M. and Liew, F. Y. 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., Wei, X., Liew, F. Y. and Brock, J. H. 2002. Regulation of phagosomal iron release from murine macrophages by nitric oxide. Biochemical Journal 365(1), pp. 127-132.
Khan, I. A., Moretto, M., Wei, X., Williams, M., Schwartzman, J. D. and Liew, F. Y. 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.
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.
Canthaboo, C., Xing, D., Wei, X. and Corbel, M. J. 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)

2001

Armour, K. J., Armour, K. E., van't Hof, R. J., Reid, D. M., Wei, X., Liew, F. Y. and Ralston, S. H. 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., Leung, B. P., Arthur, H. M. L., McInnes, I. B. and Liew, F. Y. 2001. Reduced incidence and severity of collagen-induced arthritis in mice lacking IL-18. The Journal of Immunology 166(1), pp. 517-521.

2000

Smith, X. G., Bolton, E. M., Ruchatz, H., Wei, X., Liew, F. Y. and Bradley, J. A. 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.
Leung, B. P., Wei, X., Arthur, H., Gracie, A., Robertson, S., Liew, F. Y. and McInnes, I. B. 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)
van't Hof, R. J., Armour, K. J., Smith, L. M., Armour, K. E., Wei, X., Liew, F. Y. and Ralston, S. H. 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)
McInnes, I. B., Gracie, J. A., Leung, B. P., Wei, X. and Liew, F. Y. 2000. Interleukin 18: a pleiotropic participant in chronic inflammation. Immunology Today 21(7), pp. 312-315. (10.1016/S0167-5699(00)01648-0)
Leung, B. P., McInnes, I. B., Esfandiari, E., Wei, X. and Liew, F. Y. 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., Goodridge, H. S., Harnett, M. M., Wei, X., Nikolaev, A. V., Higson, A. P. and Liew, F. Y. 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., Paterson, J. C. M., Wei, X., Liew, F. Y., Garside, P. and Kennedy, M. W. 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., Erwig, L., Wei, X., Liew, F. Y., Rees, A. J. and Savill, J. S. 2000. Activated macrophages direct apoptosis and suppress mitosis of mesangial cells. The Journal of Immunology 164(4), pp. 2110-2119.

1999

McInnes, I. B., Leung, B. P., Ruchatz, H., Field, M., Wei, X., Gemmell, C. G. and Liew, F. Y. 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.
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.
Millar, A. E., Sternberg, J., McSharry, C., Wei, X., Liew, F. Y. and Turner, C. M. R. 1999. T-cell responses during Trypanosoma brucei infections in mice deficient in inducible nitric oxide synthase. Infection and Immunity 67(7), pp. 3334-3338.
Feng, G., Goodridge, H. S., Harnett, M. M., Wei, X., Nikolaev, A. V., Higson, A. P. and Liew, F. Y. 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.
Niedbala, W., Wei, X., Piedrafita, D., Xu, D. and Liew, F. Y. 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)

1998

Ruchatz, H., Leung, B. P., Wei, X., McInnes, I. B. and Liew, F. Y. 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., Xu, D., Esfandiari, E., Sands, W., Wei, X. and Liew, F. Y. 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.
MacLean, A., Wei, X., Huang, F. P., Al-Alem, U. A. H., Chan, W. L. and Liew, F. Y. 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.
Cattell, V., Cook, H. T., Ebrahim, H. B., Waddington, S. N., Wei, X., Assmann, K. J. M. and Liew, F. Y. 1998. Anti-GBM glomerulonephritis in mice lacking nitric oxide synthase type 2. Kidney International 53(4), pp. 932-936.
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., Leung, B., Wei, X., Gemmell, C. C. and Liew, F. Y. 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., Wei, X., Gracie, J. A., Thomson, J., Liew, F. Y. and Bradley, J. A. 1996. Allograft rejection by mice lacking inducible nitric oxide synthase. Immunology 89, pp. ORI24-ORI24.
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.
Proudfoot, L., Nikolaev, A. V., Feng, G. J., Wei, X., Ferguson, M. A. J., Brimacombe, J. S. and Liew, F. Y. 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.
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., Wei, X., Liew, F. Y., Moncada, S. and Charles, I. G. 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)

Diddordebau ymchwil

Mae cytokines yn chwarae rhan ganolog wrth reoli canlyniad clefydau heintus ac ymfflamychol trwy reoleiddio imiwnedd cynhenid ac addasol gwesteiwr. Mae fy ymchwil wedi canolbwyntio ar ddeall rôl rhai cytocinau pro-llidiol pwysig, megis IL-15, IL-18, IL-12, IL-23, IL-27 a'r cytocinau gwrthlidiol newydd, IL-34 ac IL-35, mewn prosesau clefydau er mwyn dod o hyd i ffyrdd ymarferol o reoleiddio ymatebion imiwnedd cynnal ar gyfer triniaeth. Mae cytocinau llidiol yn hyrwyddo imiwnedd cynnal yn erbyn goresgyniad pathogen a ffurfio tiwmorau. Fodd bynnag, mae gorymateb hefyd yn arwain at glefydau hunanimiwn ac llidiol, fel arthritis gwynegol a chlefydau periodontal. Mae celloedd cynnal yn cynhyrchu cytocinau gwrthlidiol i osgoi'r goradwaith hwn. Un o'r cytocinau gwrthlidiol pwysig hyn yw IL-35. Rwy'n un o'r ymchwilwyr arloesol a ddarganfu IL-35 a nododd ei rôl gwrthlidiol gan ddefnyddio model arthritis gwynegol llygoden. Mae fy ymchwil yn parhau i ddeall rôl IL-35 mewn clefydau dynol eraill fel ymgeisyddiaeth, datblygu tiwmorau a dirywiad niwronau. Trwy ddeall mecanweithiau biolegol IL-35 mewn clefydau dynol, gellir cyflawni datblygiad therapïau i drin y clefydau dynol hynny.

Mae macroffagau preswyl meinwe yn meddiannu 5-10% o gydran celloedd meinweoedd ac yn chwarae rolau pwysig wrth gael gwared â chelloedd marw a chynhyrchu cytokine yn ystod prosesau clefydau. Mae macroffagau meinwe yn heterogenaidd iawn ac yn arddangos plastigrwydd. Bydd meinweoedd llidiol gyda sytocinau pro-llidiol uwch yn cymell macroffagau i'w ffenoteip M1, tra mewn amgylchedd gwrthlidiol gyda lefelau uwch o ffactorau twf a sytocinau gwrthlidiol, mae trosi i ffenoteip M2 yn cael ei ffafrio. Nod fy ymchwil yw penderfynu sut mae'r amgylchedd meinwe yn ymgorffori'r trawsnewidiad ffenoteip macrophage hwn a sut mae'r macroffagau hyn yn cyfrannu at ganlyniad clefydau dynol, gan gynnwys candidosis, datblygu tiwmorau, dirywiad niwronau ac atgyweirio meinweoedd. Mae brechlynnau'n offer effeithiol wrth baratoi'r system imiwnedd letyol i'w hamddiffyn rhag ymosodiad pathogen. Mae cytokines hefyd yn chwarae rhan allweddol yn ystod y brechiad. Mae datblygu celloedd T mewn amgylchedd cytokine penodol yn pennu'r mathau o imiwnedd, hy imiwnedd cellog neu humoral. Mae llawer o fethiannau brechu yn deillio o ysgogi'r ymatebion imiwnedd math anghywir. Mae imiwnedd cyfryngol celloedd yn gwbl hanfodol ar gyfer llwyddiant rhywfaint o frechiad. Ar hyn o bryd, rwy'n gweithio ar ddatblygu proses frechu sy'n cyfuno cytocinau â symbyliad corfforol, nanoronyn a system cyflenwi micronodwyddau. Dylai'r protocol a'r ddyfais newydd ar gyfer brechu fod yn fuddiol iawn wrth hyrwyddo iechyd pobl.

Prosiectau cyfredol

Astudio rôl cytocinau newydd, IL-35, wrth reoleiddio ymateb imiwnedd gwesteiwr yn erbyn tiwmor a haint burum.

Astudio rôl cytokine IL-35 newydd mewn atheroscerosis.

Astudio rôl ddylanwadol cytokine IL-35 mewn haint niwmonia a COVID-19.

Ar wahân i ymchwil a wnaed yn yr Ysgol Deintyddiaeth, Prifysgol Caerdydd, mae Dr. Wei hefyd yn gyfrifol am addysgu ar y cwrs ecosystem lafar ar gyfer myfyrwyr BDS blwyddyn 2. Mae'n ymwneud ag archwilio ac asesu'r cwrs hwn. Mae gan Dr Wei hefyd rôl asesu mewn Dysgu Seiliedig ar Dîm (TBL). Yn ddiweddar, mae wedi cymryd rôl arweiniol enghreifftiol ym mentoriaeth myfyrwyr blwyddyn 2 ar ôl cyflwyno ac asesu. Mae Dr Wei hefyd yn goruchwylio prosiectau myfyrwyr BDS blwyddyn olaf. Mae hefyd yn helpu i gydlynu prosiect ymchwil y flwyddyn olaf mewn ysgol ddeintyddol.

Graddiodd Dr. Xiao-Qing Wei mewn meddygaeth o Ysgol Feddygol Prifysgol Peking (Prifysgol Feddygol Beijing) yn Beijing, Tsieina, a bu'n gweithio yn Sefydliad Ymchwil Hepatitis Beijing yn Ysbyty Youan, lle cynhaliodd ymchwil ar glefydau heintus, yn enwedig hepatitis. Ymunodd â grŵp imiwnoleg ym Mhrifysgol Glasgow i ymchwilio i rôl ocsid nitrig anwythadwy (iNOS) mewn heintiau ac imiwnedd ac enillodd PhD ym Mhrifysgol Glasgow. Mae ei ymchwil ôl-ddoethurol wedi canolbwyntio ar ymchwilio i rôl rhai cytocinau pwysig fel IL-15, IL-18, IL-23 ac IL-27 yn natblygiad celloedd T. Prif nod ei ymchwil mewn clefydau heintus ac awtoimiwn yw datblygu therapi gwrth-cytokine ymarferol i drin yr anhwylder llidiol, fel arthritis gwynegol (RA). Fel Uwch Gymrawd Ymchwil, cefnogwyd ei ymchwil gan Arthritis Research UK i astudio swyddogaeth IL-18 a'i dderbynyddion mewn RA. Yn ystod y cyfnod hwnnw, defnyddiodd Dr Wei ei ymchwil i astudio mecanwaith gwrth-lid. Mae Dr Wei yn ymchwilydd arloesol wrth ddarganfod IL-35 a dangosodd ei rôl atal imiwnedd wrth drin y llid ar y cyd ym model arthritis colagen llygoden, sy'n dynwared arthritis gwynegol mewn bodau dynol yn agos. Cyfrannodd ei astudiaeth IL-35 yn sylweddol at y ddealltwriaeth o fecanweithiau clefydau llidiol a gallai hefyd elwa mewn therapïau ar gyfer anhwylderau hunanimiwn ac ymfflamychol dynol yn y dyfodol. Fe'i penodwyd gyntaf yn Ddarlithydd yn yr Ysgol Deintyddiaeth, Prifysgol Caerdydd ac fe'i dyrchafwyd yn Uwch Ddarlithydd. Mae ymchwil gyfredol Dr Wei bellach yn canolbwyntio ar astudio rôl cytocinau IL-34 ac IL-35 newydd wrth reoleiddio imiwnedd cynnal, yn enwedig o ran macroffagau meinwe a haintCandida , goroesi tiwmorau, brechlyn croen a gwella clwyfau croen/asgwrn cefn. Mae ganddo ddiddordeb hefyd mewn astudio swyddogaethau cymdeithasau cytokine gyda dinistrio meinwe mwynol sy'n gysylltiedig ag RA, osteoarthritis a chlefydau periodontal.

Anrhydeddau a dyfarniadau

MB BCh, Ysgol Feddygol Prifysgol Peking (Prifysgol Feddygol Beijing) PhD, Prifysgol Glasgow

Teitl: Bioleg Foleciwlaidd a Gwyddor Protein: Nodweddu derbynyddion IL-35 ar gyfer rhwymo cytokine i greu derbynnydd hydawdd decoy ar gyfer therapi tiwmor

Mae Interleukin-35 (IL-35) yn aelod cytokine newydd o deulu IL-12 ac mae ganddo rôl atal imiwnedd mewn anhwylderau llidiol, gan gynnwys gwella clwyfau a datblygu tiwmorau. Mae macroffagau yn arddangos plastigrwydd ar gyfer newid eu ffenoteipiau i'w hamgylcheddau meinwe. Er enghraifft, mae macroffagau llidiol M1 yn codi mewn llid ar gyfer effeithiau tiwmor neu mae macroffagau gwrthlidiol M2 yn digwydd wrth ddatrys llid yn ystod twf tiwmor a metastasis. Yn ddiweddar, rydym wedi dangos y gall IL-35 drosi M1 yn facrophages M2 i hyrwyddo datblygiad tiwmorau. Mae'r ddau tiwmor a'r rheolydd ymdreiddio T cell (Treg) yn cynhyrchu IL-35. Mae mynegiant IL-35 uwch mewn tiwmorau yn arwain at dwf tiwmor a metastasis, sy'n gysylltiedig ag ehangu macrophage M2 mewn tiwmorau. Mae IL-35 yn rhwymo i gp130 ac IL-12Rb2 ar gyfer ei weithgaredd biolegol. Gall IL-35 ddefnyddio homodimer gp130, homodimer IL-12Rb2 a heterodimer gp130 / IL-12Rb2 i gymell ei weithgaredd biolegol trwy phosphorylation o ffactorau trawsgrifio genynnau STAT1, 3, a 5 yn y drefn honno. Mae mecanweithiau (au) manwl o sut mae IL-35 yn atal ymatebion imiwnedd mewn llid yn parhau i fod yn anhysbys. Hefyd, ni astudiwyd cyfuniad o'r defnydd o dderbynyddion ar gyfer rhwymo IL-35 affinitive a phenodol uwch. Rhagdybiaeth y prosiect arfaethedig hwn yw bod heterodimer gp130 ac IL-12Rβ2 yn darparu cysylltiad uchaf sy'n rhwymo i IL-35. Bydd gp130 / IL-12Rβ2 hydawdd decoy yn blocio IL-35 yn benodol y gellir ei ddefnyddio mewn therapi tiwmor. Bydd y prosiect hwn yn nodweddu'r derbynnydd IL-35 am ei rwymiad ligand ac yna adeiladu derbynnydd decoy IL-35 hydawdd i rwystro gweithgaredd biolegol IL-35. Gellir defnyddio'r atalydd IL-35 penodol hwn hefyd wrth astudio'r IL-35 mewn clefydau eraill, fel atherosclerosis ac anhwylderau hunanimiwn.

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WeiX1@caerdydd.ac.uk
+44 29225 10648

Dr Xiao-Qing Wei

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Dr Xiao-Qing Wei

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