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MMI Faculty

Debby Burshtyn, PhD

D. Burshtyn
Dept. of Medical Microbiology & Immunology
University of Alberta
Faculty of Medicine & Dentistry
6-142E Katz Group Centre
T6G 2E1 Edmonton, AB

Ph : (780) 492-0646
Fx : (780) 492-7521

**Please note that Dr. Debby Burshtyn is not accepting any students at this time**


  • Professor, Dept. of Medical Microbiology and Immunology (2016 - )
  • Associate Professor, Dept. of Medical Microbiology and Immunology
    Graduate Coordinator (2009 - 2016)
  • Li Ka Shing Institute of Virology (2010 - )
  • Leader – Human Immunology at uAlberta Node (CHIN) (2012 -)
  • Associate Editor - The Journal of Immunology (2010-)
  • Review Editor - Frontiers in NK Cell Biology (2011-)
  • Alberta Innovates – Health Solutions Senior Scholar (2006-2014)
  • Lougheed Fellow (2000-2005)
  • CHIR New Investigator (2000-2005)
  • Alberta Heritage Foundation for Medical Research Scholar (1999-2005)

Research Areas:

My research program encompasses studies of the cell and molecular biology of several receptors that regulate Natural Killer (NK) cells and viral regulation of the ligands of these receptors.

• The human Leukocyte Receptor Complex encodes two families of highly related receptors known as Leukocyte Immunoglobulin-like Receptors (LILRs) and Killer Cell Immunoglobulin-like Receptors (KIRs) that regulate immune function.
• These highly polymorphic gene families encode activating and inhibitory receptors expressed in distinct patterns on immune cells.
• Many of these receptors bind to proteins involved in antigen presentation known as MHC-I (Major Histocompatibility Class I Molecules).
• The vast diversity of these receptors is believed to be driven by balancing forces that select for receptors that retain their physiologic function of immune regulation by binding MHC-I proteins, but avoid immune evasion mechanisms of pathogens.
• KIRs are selectively expressed by NK cells.
• KIR genotype in combination with MHC-I genotype plays a role in an individual’s resistance to human pathogens such as HIV and Hepatitis C virus.
• LILRs are widely expressed by many different types of immune cells
• Polymorphism in LILRs have been linked to susceptibility to autoimmune diseases such as Rheumatoid Arthritis, Systemic Lupus Erythmatosis and Multiple Sclerosis.
• Cytomegalovirus contains a protein that binds tightly to one of the LILR family members known as LILRB1.
• LILRB1 is expressed by many immune cells including NK cells and monocytes.

We currently have projects funded by CIHR and LKS Institute of Virology to study the functional regulation of the receptor LILRB1 and viral disruption of host proteins used by NK cells to determine the health of a cell.

Leukocyte Ig-Like Receptor-B1 Regulation and Function
By increasing our understanding of LILRB1 in general, and by examining how natural polymorphisms influence LILRB1 function in particular, we hope to gain insight into how this receptor is involved in variation of the immune response between individuals.

The resulting information may have value for the development of prognostic indicators to better target treatments and strategies to exploit this pathway for vaccine development and therapies. We currently have two main ongoing projects studying LILRB1.


Project 1. Regulation of LILRB1 gene expression.
LILRB1 expression is consistent between individuals on most immune cells types including myeloid and B lymphocytes. However the extent of LILRB1 expression on natural killer cells ranges from 25-75% depending on the person. We previously showed that higher expression in natural killer cells correlates with one of two major genotypes in the population and that it is related to transcription of the gene into messenger RNA. The goal of this study is to determine how transcription of the LILRB1 gene is regulated to determine why one major haplotype is more highly expressed by natural killer cells while there is no difference manifested in B cells. For these studies we are investigating the basic transcriptional and epigenetic regulation of the gene as well as epigenetic regulation.

Project 2. LILRB1 genetic variation, cytomegalovirus and UL18.
Human cytomegalovirus is widespread in the population and typically is a persistent but asymptomatic infection. However, CMV is a major clinical complication following organ transplantation, it is also associated with development of cardiovascular disease and remains a major cause of birth defects if a primary infection is acquired during pregnancy. We are testing if variation in LILRB1 is related to susceptibility to cytomegalovirus disease post transplantation. In a related study, we are testing the hypothesis that UL18 binds to LILRB1 within infected cells to disrupt normal LILRB1 signalling.

Modulation of NK-ligands by Viruses

We are studying two distinct receptor-ligand combinations with two different viral models to understand the molecular mechanisms underlying NK cell recognition of virus-infected cells.

Project 1. Poxvirus effects on C-type Lectin receptors and ligands. Poxviruses have garnered much attention in recent years due to fears of their use as a biological weapon as well as their potential usefulness as a vaccine vector and for tumor therapy. Natural killer cells are established as providing resistance to poxvirus infection in certain strains of mice. While poxviruses dramatically disrupt host protein synthesis only a small subset poxviruses actively suppress expression of MHC-I expression that could lead to activation of natural killer cells. This raises the question of whether proteins other than MHC-I are altered during infection by a poxvirus to alert natural killer cells. Recently, we described loss of the protein Clr-b from the cell surface following poxvirus infection of mouse cells. Clr-b is widely expressed protein that prevents natural killer cell activaty through the receptor NKRP1B. Our future goals are to establish the mechanism leading to the downregulation of Clrb as well as extend the studies to the human equivalent.

Project 2. The effect of Hepatitis C on MHC-I
Hepatitis C, a virus that establishes persistent infection in ~80% of those exposed leading to liver disease and hepatic cancer. Epidemiological studies suggest that the KIR receptor system is important in natural resistance to Hepatitis C, but there is little evidence to suggest that Hepatitis C infection influences expression of MHC-I. Recent progress in propagation of Hepatitis C in vitro has enabled us to begin to study how acute infection with Hepatitis C alters MHC-I expression in vitro. Preliminary experiments suggest acute infection does reduce cell surface MHC-I. Studies are ongoing to determine the viral proteins involved and to extend these studies to infected cells in a humanized mouse liver model.

If you are interested in postdoctoral studies please submit a CV including contact information for 3 references and a brief description of how your background and education fit with our laboratory interests.

If you are interested in graduate studies please send by email a brief description of your background research experience, future career goals and a copy of your transcripts.  

Further information regarding the MMI graduate program can be found through the MMI Homepage.



  • Chelsea Davidson (Graduate Student)
  • Chris Morcos (Graduate Student)
  • Kinola Williams (Graduate Student)
  • Kang Yu (Graduate Student)



Click here for most recent publications


Selected Publications:

  1. Poxvirus Infection-Associated Downregulation of C-Type Lectin-Related-b Prevents NK Cell Inhibition by NK Receptor Protein-1B. Williams KJ, Wilson E, Davidson CL, Aguilar OA, Fu L, Carlyle JR, and DN Burshtyn. 2012 Journal of Immunology 188:4980-91 (CIHR 36344)

  2. Montgomery, B.C, Cortes, H.D., Burshtyn, D.N., and J.L. Stafford. Channel catfish leukocyte immune-type receptor mediated inhibition of cellular cytotoxicity is facilitated by SHP-1-dependent and -independent mechanisms.  2012  Developmental & Comparative Immunology 37:151-163  (CIHR 36344)

  3. Li, N.L., Davidson, C.E., Humar, A. and D.N. Burshtyn.  Modulation of the inhibitory receptor leukocyte Ig-like receptor 1 on human natural killer cells.  Frontiers in NK Cell Biology, available on line Sept 06, 2011. (CIHR 36344)

  4. The first Ig-domain of KIR3DL1 contacts MHC-I at a secondary site.  Fu, L., Hazes B. and D.N. Burshtyn, 2011 Journal of Immunology 187:1816-25  (CIHR 36344)

  5. Davidson, C., Li, N. and D.N. Burshtyn. LILRB1 polymorphism and surface phenotype of natural killer cells.  2010 Human Immunology 71:942.  (CIHR 36344)

  6. Osman, MS, Burshtyn, DN, Kane, KP. Activating Ly-49 receptors regulate LFA-1-mediated adhesion by NK cells. J Immunol 2007 Feb 1;178(3):1261-7

  7. Kirwan,  SE, Burshtyn, DN.  Regulation of natural killer cell activity.
    Curr Opin Immunol. 2007 Feb;19(1):46-54

  8. Treanor, B, Lanigan, PM, Kumar, S, Dunsby, C, Munro, I, Auksorius, E, Culley, FJ, Purbhoo, MA, Phillips, D, Neil, MA, Burshtyn, DN, French, PM, Davis, DM. Microclusters of inhibitory killer immunoglobulin-like receptor signaling at natural killer cell immunological synapses.  J Cell Biol. 2006 Jul 3;174(1):153-61

  9. Kirwan, S, Merriam, D, Barsby, N, McKinnon, A, Burshtyn, DN. Vaccinia virus modulation of natural killer cell function by direct infection. Virology. 2006 Mar 30;347(1):75-87

  10. Kirwan, SE, Burshtyn, DN. Killer cell Ig-like receptor-dependent signaling by Ig-like transcript 2 (ILT2/CD85j/LILRB1/LIR-1).J Immunol. 2005 Oct 15;175(8):5006-15

  11. Standeven, LJ, Carlin, LM, Borszcz, P, Davis, DM, Burshtyn, DN. The actin cytoskeleton controls the efficiency of killer Ig-like receptor accumulation at inhibitoryNK cell immune synapses. J Immunol. 2004 Nov 1;173(9):5617-25