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 d�Hennezel, 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. d�Hennezel 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?
|