Maziar Divangahi

photo of maziar divangahi: research on Host defense against pulmonary pathogens, influenza, tuberculosisPosition
Associate Professor, Department of Medicine, McGill University
Associate Member, Department of Microbiology & Immunology, McGill University

Publications  pubmed link for maziar divangahi publications

Currently accepting graduate students and postdoctoral fellows

Article in International Innovation*

Research Interests

  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.

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Contact Information

Meakins-Christie Laboratories
RI-MUHC, Block E
Office EM2.2248
Lab E03.2371
1001 Decarie Blvd.
Montreal QC H4A 3J1

Tel: 514-934-1934 Ext. 76237 (lab)
Tel: 514-934-1934 Ext. 76413 (office)
Tel: 514-934-1934 Ext. 76172 (admin)
Fax: 514-933-3962


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