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CIHR Skin Research Training Centre
Core Mentors: Dr. Jan Dutz
Dutz, Jan Peter, MD, FRCPC
Scientist Level 3, CFRI
Professor, Department of Dermatology and Skin Science, University of British Columbia
Affiliate Member, Department of Medicine, University of British Columbia

Room A4-144, 950 West 28th Avenue
Vancouver, BC V5Z 4H4 
Tel: 604-875-4747
Fax: 604-873-9919 (office); 604-875-3597 (lab)
Website: http://www.skincarecentre.ca/about_us/doctors/jan_dutz.htm
Email: dutz@interchange.ubc.ca
                         

Education

1983 MD Queen's University, Kingston, ON
July 1983 - June 1984 Internship Toronto East General Hospital, ON
July 1984 - June 1986 Resident 1 & 2 Toronto General Hospital, ON
July 1986 - June 1987 Resident 3 St. Michael's Hospital, Toronto, ON
July 1987 - June 1988 Rheumatology Fellow 1 Wellesley Hospital, Toronto, ON
July 1988 - July 1989 Rheumatology Fellow 2 Toronto General Hospital, ON
July 1994 - Jan 1997 Resident University of British Columbia 

Awards and honors

2001 Martin M Hoffman Award for Excellence in Research, University of British Columbia Department of Medicine
2000 Junior Scholar, Arthritis Society of Canada 

Grant Support

Canadian Dermatology Foundation 
Arthritis Society of BC
B.C. Research Inst. for Child & Family Health
Faculty of Medicine UBC
BC Children's Hospital Foundation New Research Fund
UBC Heighway Fund
MRC/CIHR - Juvenile Diabetes Foundation International
Medical Research Council/CIHR
INEX Pharmaceuticals
Health Market International
The Arthritis Society
Canadian Diabetes Association 
National Cancer Institute of Canada
Canadian Foundation for Innovation
Canadian Institutes for Health Research
National Alopecia Areata Foundation
3M Pharmaceuticals
Juvenile Diabetes Research Foundation International 

Research interest

Vaccination is one of the most efficient and cost-effective methods of promoting health. Immunization as a possible treatment for cancer is a recent concept. One of the limitations of current vaccine protocols is inefficient priming for cytotoxic T lymphocytes, which are important in the control of viral infections and tumours. Skin dendritic cells are potent antigen presenters to the immune system. However, the skin historically has been regarded as a barrier and has not been intensively studied as an organ of immunization.
Our laboratory is engaged in studies to optimize the use of the skin as an organ to alter systemic immune responses. In separate projects, we are studying the priming or activation of T cells involved in models of systemic lupus erythematosus and juvenile onset diabetes mellitus.
Current projects:

1. Epicutaneous modulation of T cell function
Recent evidence suggests that proteins or peptides can be applied on intact skin to vaccinate and produce both an antibody and a T cell response. Epicutaneous immunization (that is, on intact skin) offers potential for the development of tumour and virus-specific vaccines. In addition, it may be more cost effective as well as easier to administer than current methods of immunization. We are studying the epicutaneous application of peptides and proteins and methods to enhance their delivery and immunogenicity. In addition to being an ideal organ for the initiation of immune responses, the skin can suppress immune responses. It is particularly effective in this regard after exposure to ultraviolet light. Consequently, we are also studying how the skin may be used to induce tolerance and thereby possibly treat autoimmune disease.

2. SLE, UV light and T cell priming in the skin
Systemic lupus erythematosus (SLE) is an autoimmune disorder that can have devastating consequences. Lupus often begins in the skin and can worsen with exposure to sunlight. Recent experimental data in mouse models suggests that the skin may be the organ where T cells are first activated in lupus. Recent data also suggest that cytotoxic T cells may be involved in the initiation of lupus autoimmunity. A better understanding of how the skin may initiate immune responses will shed light on the role of the skin in initiating and/or perpetuating disease activity in systemic lupus erythematosus.

3. Treating diabetes by modulating cross presentation
Type 1 diabetes mellitus is an autoimmune disease in which insulin-producing cells (termed beta cells) in the pancreas are destroyed. We have determined that beta cell death in the pancreas allows beta cell antigens to be processed by specialized antigen presenting cells called dendritic cells. These dendritic cells can then activate diabetes-inducing cytotoxic T cells through a process termed cross-presentation. We are currently determining which additional factors are required for the detrimental cross-presentation of self-antigen and how this may be inhibited.

Current lab members

Mehran Ghoreishi (Research assistant/Technician)
YiQun Zhang (Research assistant/Technician)
Hossain Najar (Research associate)
Jacqueline Lai (Postdoctoral Fellow)
Roopjeet Kahlon (Graduate student)
Wing-ki (Vicki) Cheng (Graduate Student) 

Selected recent publications

  1. Vera-Kellet C, Peters L, Elwood K, Dutz JP.: Usefulness of Interferon-{gamma} Release Assays in the Diagnosis of Erythema Induratum. Arch Dermatol. 2011 Aug;147(8):949-52. PMID: 21844454
  2. Han C, Sreenivasan G, Dutz JP.: Reversible retiform purpura: a sign of cocaine use. Arch Dermatol. 2011 Aug;147(8):949-52. PMID: 21402686
  3. Lee AS, Gibson DL, Zhang Y, Sham HP, Vallance BA, Dutz JP, Gut barrier disruption by an enteric bacterial pathogen accelerates insulitis in NOD mice. Diabetologia. 2010 Apr;53(4):741-8. PMID: 20012858
  4. Ghoreishi M, Martinka M, Dutz JP: Type 1 interferon signature in the scalp lesions of alopecia areata, Br J Dermatol. 2010 Jul;163(1):57-62. PMID: 20346028
  5. Zhang Y, Lee AS, Shameli A, Geng X, Finegood D, Santamaria P, Dutz JP: TLR9 Blockade Inhibits Activation of Diabetogenic CD8+ T Cells and Delays Autoimmune Diabetes. J Immunol. 2010 May 15;184(10):5645-53. PMID: 20393135
  6. Broady R, Yu J, Chow V, Tantiworiwat A, Kang C, Berg K, Martinka M, Ghoreishi M, Dutz JP, Levings MK: Cutaneous GVHD is associated with the expansion of tissue localised Th1 and not Th17 cells. Blood. 2010 Dec 16;116(25):5748-51. Epub 2010 Sep 23. PMID: 20864580
  7. Lee AS, Ghoreishi, M, Cheng, W-K, Chang, TY, Zhang, Y, Dutz, JP: Toll-like Receptor 7 Stimulation Promotes Autoimmune Diabetes in the Non-Obese Diabetic Mouse. Diabetologia, 2011 Jun;54(6):1407-16. Epub 2011 Feb 22. PMID: 21340621
  8. de Gannes GC, Ghoreishi M, Pope J; Russell A; Bell D; Adams S; Shojania K; Martinka M, DUTZ JP: Psoriasis Triggered by Tumor Necrosis Factor-α Inhibitors in Patients with Rheumatologic Conditions. Arch Dermatol. 2007 Feb;143(2):223-31. PMID: 17310002
  9. Najar HN and DUTZ, JP: Topical TLR9 agonists induce more efficient cross-presentation of injected protein antigen than parenteral TLR9 agonists do. Eur J Immunol. 2007 Aug;37(8):2242-56. PMID: 17634951
  10. Najar HN and DUTZ, JP: Topical CpG enhances the response of murine malignant melanoma to dacarbazine. J Invest Dermatol, 2008 Sep;128(9):2204-10. Epub 2008 Mar 27. PMID: 18368132
  11. Ghoreishi M, Bach P, Obst J, Komba M, Fleet JC, DUTZ JP: Expansion of antigen-specific regulatory T cells with the topical vitamin D analogue calcipotriol. J Immunol. 2009 May 15;182(10):6071-8.PMID: 19414758
  12. Chang BA, Cross JM, Najar HM, DUTZ JP: Topical resiquimod promotes priming of CTL to parenteral antigens. Vaccine. 2009 Sep 25;27(42):5791-9. Epub 2009 Aug 4. PMID: 19660592

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