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 Home / About Us > Dr Ciriaco Piccirillo

Contact info

Dr Ciriaco A. Piccirillo
MUHC ∑ Montreal General Hospital
1650, Cedar Avenue - Room L11.132-144
Montreal, QC H3G 1A4

Tel: 1-514-934-1934, ext. 45135
Fax: 1-514-934-8332
E-mail: ciro.piccirillo@mcgill.ca

Link to Piccirillo Lab webpage

 

Research keywords

  • Immune regulation
  • Autoimmune diseases
  • Type 1 diabetes
  • Foxp3+ regulatory T cells
  • T cell biology
  • Immunotherapy
  • Immune suppression
  • Chronic inflammatory disorders

 

Ciriaco A. Piccirillo, PhD
Associate Professor of Microbiology & Immunology
Canada Research Chair in Regulatory Lymphocytes of the Immune System


Biographical Sketch

Dr Piccirillo is a reputed immunologist who trained at the reputed Laboratory of Immunology, National Institute of Allergy and Infectious Diseases (NIAID), National Institutes of Health (NIH, Bethesda, USA). He is Associate Professor in the Department of Microbiology and Immunology, and Director of the Laboratory of Immunoregulation at the Faculty of Medicine of McGill University. He is currently co-Leader of the Infection and Immunity Axis at the Research Institute of the McGill University Health Center. He is also the Director of McGill's FOCIS Center of Excellence in Translational and Clinical Immunology whose mission is to support basic and clinical research in immunology.

Dr Piccirillo's research program as Canada Research Chair in Regulatory lymphocytes of the Immune System focuses on the regulation of immune responses mediated by CD4+Foxp3+ regulatory T cells, a unique population of cells viewed as the central master-regulators of the immune system in mice and humans. His research is responsible for many seminal studies related to the phenotype, function and mechanism of action of Treg cells in a variety of animal models, non-human primates and humans.

His research program may lead to the development of novel immunotherapeutic strategies to manipulate CD4+Foxp3+ Treg cell function and ultimately modulate autoimmune and chronic inflammatory diseases. His research has received an international reputation, as reflected by the numerous publications in high impact journals, invitations to many national and international scientific meetings, solicitations to consult for companies, government and associations, to serve as reviewer to major scientific journals, and also to the Committee on Pathogenesis and Functional Genomics of the TDR branch/WHO.


Selected Scientific Contributions

1. McHugh RS, MJ Whitters, CA Piccirillo, DA Young, EM Shevach, M Collins and MC Byrne. Gene expression analysis of CD4+ CD25+ immunoregulatory T cells: A unique cell phenotype and a functional role for the Glucocorticoid-induced TNF receptor. Immunity 16:311-23, 2002.

2. Piccirillo CA, JJ Letterio, AM Thornton, RS McHugh, M Mamura, H Mizuhara and EM Shevach. CD4+CD25+-mediated suppression of T cell activation in vitro is independent of TGF-β1 production and responsiveness. J Exp Med 196:237-46, 2002.

3. Belkaid Y*, CA Piccirillo*, S Mendez, EM Shevach and DL Sacks. CD4+CD25+ regulatory T cells control Leishmania major persistence and immunity. Nature 420:502-7, 2002. *Co-first author

4. Piccirillo CA and EM Shevach. FOCUS-Viewpoint article "CD4+CD25+ immunoregulatory T cells: naturally-occurring but adaptable." Nature Rev Immunol 3, 2003.

5. Yurchenko K, M Tritt, V Hay, Y Belkaid and CA Piccirillo. CCR5-dependent recruitment of naturally-occurring CD4+CD25+ regulatory T cells in sites of chronic infection favors pathogen persistence. J Exp Med 203:2451-60, 2006.

6. Tritt M, E Sgouroudis, E díHennezel, A Albanese and CA Piccirillo. Functional waning of naturally-occurring CD4+ regulatory T cells contributes to the onset of autoimmune diabetes. Diabetes 57:113-23. 2008.

7. Tang Q, JY Adams, C Penaranda, K Grossheider, E Piaggio, E Sgouroudis, CA Piccirillo, BL Salomon and JA Bluestone. Central role of a defective IL-2 production in triggering islet autoimmune destruction. Immunity 28:687-97, 2008.

8. Sgouroudis E, A Albanese and CA Piccirillo. Functional impact of Idd3 alleles on the development of naturally-occurring CD4+Foxp3+ regulatory T lymphocytes and resistance to autoimmune diabetes. J Immunology 181:6283-92, 2008.

9. d'Hennezel E, M Ben-Shoshan, HD Ochs, TR Torgerson, LJ Russell, C Lejtenyi, FJ Noya, N Jabado, B Mazer and CA Piccirillo. Functional evaluation of regulatory T cells in IPEX caused by a missense mutation in the FOXP3 forkhead domain. NEJM 361:1710-3, 2009.

10. Piccirillo CA. Treg's Alter Ego: An Accessory in Tumor Killing. Immunity 33:838-40, 2010.

11. Sgouroudis E, M Kornete and CA Piccirillo. IL-2 allelic variation modulates dendritic cell-mediated potentiation of CD4+Foxp3+ regulatory T cell function and resistance to autoimmune diabetes. Autoimmunity 44:406-14, 2011.

12. díHennezel E, E Yurchenko, E Sgouroudis, V Hay and CA Piccirillo. Single-cell analysis of the human TREG population uncovers functional heterogeneity and instability within FOXP3+ cells. J Immunology 186:6788-97, 2011.

13. Kornete M and CA Piccirillo. Critical co-stimulatory pathways in the stability of Foxp3+ Treg cell homeostasis in Type I Diabetes. Autoimmunity Rev 2011 (in press).

14. Liston A and CA Piccirillo. Functional plasticity in Foxp3+ regulatory T cells. Nature Med 2011 (in press).

Click here for PubMed listing


Research Interests

The Piccirillo laboratory makes use of cutting-edge experimental strategies to characterize the relative contribution of CD4+Foxp3+ Treg cells as a natural checkpoint in establishing resistance or susceptibility to immune-mediated disorders. The primary focus of his research is to characterize the functional dynamics of CD4+Foxp3+ Treg cell activity in human autoimmune diseases (type 1 diabetes) as well as in animal models of autoimmunity (type 1 diabetes), tumors (spontaneous breast cancer), infections (malaria), and mucosal immunity (inflammatory bowel disease). His research program makes use of standard and state-of-the-art molecular, cellular and imaging approaches to characterize the behavior of CD4+Foxp3+ Treg cells in health and disease.

The research program in the laboratory falls into 5 specific areas:

1. Is Foxp3+ Treg cell function stable in vivo?

2. What is the functional dynamics of Foxp3+ Treg cell in lymphoid and non-lymphoid tissues in health and disease?

3. Is there a Foxp3+ Treg cell dysfunction in inflammatory conditions, like type 1 diabetes?

4. How does genetic variation impact Foxp3+ Treg cell function in type 1 diabetes?

5. What is the transcriptional and translational regulation of gene expression in pathogenic and regulatory T cell subsets?

   
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