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 Maziar Divangahi

Maz
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Position

Asst Prof, Dept Medicine
Assoc Member, Dept Micro & Immunol
McGill University

Contact Information

Meakins-Christie Labs
McGill University
3626 St. Urbain Street
Montreal , Quebec H2X 2P2 Canada

Tel: 514-398-3864 x089727
Fax: 514-398-7483
E-Mail: maziar.divangahi@mcgill.ca

Education & Training

BSc (Biol) McMaster, 2000
PhD (Immunol), McGill,
   2005
PDF (Inf Dis), McMaster,
   2007
PDF (Innate Immunity)
   McGill, 2008
PDF (Macrophage Death)
   Harvard, 2010
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Publications: PubMed


Currently accepting graduate students & postdoctoral fellows

 

Research Interests

Recent article in International Innovation*

  1. To understand the cellular and molecular mechanisms of host defense against Influenza and Mycobacterium tuberculosis
  2. To unravel the mechanisms by which PAMPs and eicosanoids regulate the macrophage death program
  3. To define the consequences of macrophage death modality on T cell mediated immunity
  4. To design a new generation of vaccines using recombinant or deleted gene based organisms and/or in combination with host eicosanoids modulation

The goal of my research program is to investigate the cross-talk between innate and adaptive immunity against two intracellular pulmonary pathogens, influenza and Mycobacterium tuberculosis (Mtb). Antigen presenting cells, such as macrophages or dendritic cells, fine-tune immune responses, by instructing an effective level of activation, proliferation, and differentiation of naïve T cells. One mechanism by which virulent pathogens successfully inactivate host defense mechanisms is by interrupt the cross-talk between innate and adaptive immunity. APC initially sense pathogens through pathogen-associated molecular patterns (PAMPs) including Toll-like receptors (TLRs) and Nod-like receptors (NODs). This initial recognition induces a cascade of inflammatory responses including cytokine/chemokine induction and recruitment of inflammatory cells to the site of infection. However, the pathogen-driven inflammatory response needs to be tightly regulated by the host to prevent immune-pathology. Eicosanoids play an important regulatory role in the host immune response including cell death programs that directly affect both innate and adaptive immunity. There are two major cell death pathways; apoptosis and necrosis. Several pathogens hijack cell death programs to their advantage. Recently we define that eicosanoid-regulated cell death of Mtb-infected macrophages modulates both innate and T cell mediated immunity against Mtb. Necrosis is a strategy that Mtb exploit to exit from macrophages and infect other cells. In contrast, apoptosis, characterized by an intact plasma membrane, is an innate defense mechanism that reduces bacterial viability as well as enhancing T cell priming via cross-presentation of the antigen cargo of apoptotic macrophages by dendritic cells. Thus, we are interesting to understand the molecular mechanisms by which APC regulate the immune response to infectious diseases which may ultimately allow us to design better vaccine or targeted drugs against these two devastating diseases.

To achieve our research goals, we have established mouse models of influenza pneumonia and M. tuberculosis as well as primary cell cultures. The laboratory has a dedicated 11-colour flow cytometer LSR-II, an imaging technology, and the state-of-art BL2 facility, which allows us to handle BL2 pathogens, including influenza virus for both in vitro and in vivo studies. The study with Mtb is being conducted through collaboration with Dr. Marcel Behr laboratories containing BL3 facility.


*International Innovation, published by Research Media, is the leading global dissemination resource for the wider scientific, technology and research communities, dedicated to disseminating the latest science, research and technological innovations on a global level. More information and a complimentary subscription offer to the publication can be found at: www.researchmedia.eu