Dr Wuding Zhou
MRC Centre for Transplantation
King’s College London
5th Floor, Tower Wing
London SE1 9RT
Tel 0207 1881528
Fax 0207 1885660
Present Post: Reader in Immunology
About Dr Wuding Zhou
Wuding Zhou graduated from Huaxi Medical University in China in 1983 and gained a PhD in the department of Nephrology and Transplantation at Guy’s Hospital, London University in 1995. In the same department, she carried out 5 years post-doctoral research and subsequently became Lecturer in 2001 and Reader in immunology in 2009. Wuding has being working in the fields of complement and immunology since her PhD studies began.
A list of Dr Zhou’s publications and reviews can be found on the PubMed website
Wuding’s PhD and Post-doctoral studies involved the role of complement (C) in renal disease and ischemia/reperfusion (IR) injury, which have identified the cells and components involved in intra-renal synthesis of complement and their association with renal diseases, ischemia/reperfusion injury and transplant rejection. These studies have led 28 publications including Lancet, JCI. Since becoming a Lecturer in 2001 and now Reader in Immunology at King’s College London, Wuding has focused her research on the role of C as an important regulator of immune responses. Wuding is currently interested in the role of complement particularly C3a and C5a in immune regulation and trying to understand whether and how complement interacts with several pivotal cells of the immune system (e.g. antigen presenting cells, natural killer cells, macrophages and stem cells) participating in antimicrobial defence, cancer elimination, ischaemia/reperfusion injury, transplant rejection, autoimmunity and tissue repair. Understanding of the interaction between complement and these cells may lead to the development of new (complement-based) pharmaceutical approaches.
The major contributions of her group’s research to this field include the following discoveries or identifications:
• DCs, the most important antigen presenting cells (APCs) are able to synthesise a wide range of C proteins. (JI 2006, MI 2011)
• Local production and activation of C is critical for the maintenance of APC function, thus generating efficient specific T cell responses. (Blood 2006, Blood 2008)
• Anaphylatoxins (C3a, C5a) acting on their receptors expressed on DCs is an important mechanism by which C modulate adaptive immune responses. cAMP/PKA signalling is a major pathway through which C3a-C3aR or C5a-C5aR interaction modulates DC function. (Blood 2008, JI 2009, Immunobiology 2012)
• Predominant role for C5a in promoting renal IR injury. (JASN 2012)
• A contributory role for C5a receptor resulting in the rejection of organ transplants, lending support to a new therapeutic strategy to prevent rejection by blocking receptor signalling. (JASN 2010)
• A novel strategy of intragraft delivery of membrane-localising C regulator to increase the number of successful transplants in a pre-clinical model. (JASN 2006)
• C and P-selectin-mediated pathways of renal IR injury are mutually independent, suggesting that C and P-selectin pose two distinct targets for therapy (at intravascular and extravascular sites, respectively) clarifying future strategies for preventing transplant injury in clinical translation. (JASN 2004)
• C5a/C5aR signalling is an important negative regulator of NK cell homeostasis and effector function. (Manuscript in preparation)
• C5a is a critical factor in causing kidney infection and tissue damage, therefore representing a promising target for preventing and treating UTI. (Manuscript in preparation)
• Medical Research Council (MRC) project grant, 2011-14 (£447,000). Evaluating and targeting C5a receptor in pyelonephritis. W. Zhou and S. Sacks. Grant Ref: G1001141
• Medical Research Council (MRC) project grant, 2007-10 (£561,662). Receptors for C3a and C5a modify dendritic cell function in alloreactive T cell responses and allograft rejection. W. Zhou and S. Sacks. Grant Ref: G0601202
• Guy’s and St. Thomas Kidney Patients Association, 2006-07 (£10,000). Renal IR injury increases organ graft immunogenicity leading to an enhanced allo-reactive T cell response. W. Zhou.
• Wellcome Trust project grant, 2002-05 (£180,123). Complement activation pathways in renal ischemia/reperfusion injury. W. Zhou and S. H. Sacks. Grant Ref: 066960
• Alexion Pharmaceuticals Inc, 2004-05 (£46,000). The study of anti-C5 mAb for the prevention of mice from renal ischemia reperfusion injury. W. Zhou and S. H. Sacks.
• MRC PhD Studentship, 2004-07 (£57,700). Regulation of the antidonor T cell response in transplantation. Zhou W, Sacks S.
• Medical Research Council (MRC) program grant, 2007-2012 (£1,276,863). Targeting the complement system in transplantation. S. Sacks, W. Zhou, G. Lombardi. Grant Ref: G0600892
• Kidney Research UK Clinical Fellowship, 2009-12 (£192,301). Investigating a new dimension of the activating components of lectin complement pathway in kidney ischemia reperfusion injury, E Asgari, W Zhou, S Sacks. Grant Ref: TF9/2009
• Wellcome Trust project grant, 2007-2010 (£233,647). Prevention of hyperacute rejection by intra-graft delivery of membrane localising complement regulator. S. Sacks and W. Zhou. Grant Ref: 080779
• Wellcome Trust project grant, 2006-2009 (£443,321). Role of the lectin activation pathway of complement in renal reperfusion injury and transplantation. W. Schwaeble, S. Sacks, R. Sim, W. Zhou.
Recent major publications
1. Bartel G, Brown K, Phillips R, Peng Q, Zhou W, Sacks SH, Wong W. Donor specific transplant tolerance is dependent on complement receptors. Transpl Int. 2013;26:99-108.
2. Sachs SH and Zhou W: The role of complement in the early immune resposne to transplantation. Nat Rev Immunol 2012;12:433-444.
3. Peng Q, Li K, Smyth LA, Xing G, Wang N, Meader L, Lu B, Sacks SH and Zhou W: Role of C3aR and C5aR in renal ischaemia reperfusion injury. J Am Soc Nephrol 2012;23:1474-85.
4. Li K, Fazekasova H, Wang N, Peng Q, Sacks SH, Lombardi G, Zhou W: Functional modulation of human monocytes derived DCs by anaphylatoxins C3a and C5a. Immunobiology 2012;217:65-73.
5. Li K, Fazekasova H, Wang N, Sagoo P, Peng Q, Khamri W, Gomes C, Sacks SH, Lombardi G, Zhou W: Expression of complement components, receptors and regulators by human dendritic cells. Mol Immunol 2011;48:1121-1127.
6. Zhou W: The new face of anaphylatoxins in immune regulation. Immunobiology 2012;217:225-34
7. Li Q, Peng Q, Xing G, Li K, Wang N, Farrar CA, Meader L, Sacks SH, Zhou W: Deficiency of C5aR prolongs renal allograft survival. J Am Soc Nephrol 2010;21:1344-1353.
8. Peng Q, Li K, Wang N, Li Q, Asgari E, Lu B, Woodruff TM, Sacks SH, Zhou W: Dendritic cell function in allostimulation is modulated by C5aR signaling. J Immunol 2009;183:6058-6068.
9. Li K, Zhou W, Hong Y, Sacks SH, Sheerin NS: Synergy between type 1 fimbriae expression and C3 opsonisation increases internalisation of E. coli by human tubular epithelial cells. BMC Microbiol 2009;9:-64.
10. Sacks S, Lee Q, Wong W, Zhou W: The role of complement in regulating the alloresponse. Curr Opin Organ Transplant 2009;14:10-15.
11. Li K, Anderson KJ, Peng Q, Noble A, Lu B, Kelly AP, Wang N, Sacks SH, Zhou W: Cyclic AMP plays a critical role in C3a-receptor-mediated regulation of dendritic cells in antigen uptake and T-cell stimulation. Blood 2008;112:5084-5094.
12. Peng Q, Li K, Anderson K, Farrar CA, Lu B, Smith RA, Sacks SH, Zhou W: Local production and activation of complement up-regulates the allostimulatory function of dendritic cells through C3a-C3aR interaction. Blood 2008;111:2452-2461.
13. Sacks S, Zhou W: New boundaries for complement in renal disease. J Am Soc Nephrol 2008;19:1865-1869.
14. Zhou W, Patel H, Li K, Peng Q, Villiers MB, Sacks SH: Macrophages from C3-deficient mice have impaired potency to stimulate alloreactive T cells. Blood 2006;107:2461-2469.
15. Peng Q, Li K, Patel H, Sacks SH, Zhou W: Dendritic cell synthesis of C3 is required for full T cell activation and development of a Th1 phenotype. J Immunol 2006;176:3330-3341.
16. Patel H, Smith RA, Sacks SH, Zhou W: Therapeutic strategy with a membrane-localizing complement regulator to increase the number of usable donor organs after prolonged cold storage. J Am Soc Nephrol 2006;17:1102-1111.
17. Brown KM, Kondeatis E, Vaughan RW, Kon SP, Farmer CK, Taylor JD, He X, Johnston A, Horsfield C, Janssen BJ, Gros P, Zhou W, Sacks SH, Sheerin NS: Influence of donor C3 allotype on late renal-transplantation outcome. N Engl J Med 2006;354:2014-2023.
18. Farrar CA, Zhou W, Lin T, Sacks SH: Local extravascular pool of C3 is a determinant of postischemic acute renal failure. FASEB J 2006;20:217-226.
19. Li K, Patel H, Farrar CA, Hargreaves RE, Sacks SH, Zhou W: Complement activation regulates the capacity of proximal tubular epithelial cell to stimulate alloreactive T cell response. J Am Soc Nephrol 2004;15:2414-2422.
20. Farrar CA, Wang Y, Sacks SH, Zhou W: Independent pathways of P-selectin and complement-mediated renal ischemia/reperfusion injury. Am J Pathol 2004164:133-141.
21. Zhou W, Farrar CA, Abe K, Pratt JR, Marsh JE, Wang Y, Stahl GL, Sacks SH: Predominant role for C5b-9 in renal ischemia/reperfusion injury. J Clin Invest 2000;105:1363-1371.