Dr. Maziar Divangahi

Academic title(s): 

Professor - Department of Medicine, Division of Experimental Medicine
Associate Member, Department of Microbiology & Immunology

Dr. Maziar Divangahi
Contact Information
Address: 

McGill University Health Centre (MUHC)
1001 Decarie Boulevard,
Montreal, Qc, H4A 3J1

Phone: 
(514) 934-1934 ext. 76431
Email address: 
maziar.divangahi [at] mcgill.ca
Current research: 

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 interrupting 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 defined 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 exploits 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 interested in understanding the molecular mechanisms by which APC regulate the immune response to infectious diseases which may ultimately allow us to design better vaccines or targeted drugs against these two devastating diseases. 

To achieve our research goals, we  have established mouse models of influenza pneumonia and M. tuberculosisas 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 a collaboration with Dr. Marcel Behr in his laboratories containing a BL3 facility.

Projects: 

1. Understanding the cellular and molecular mechanisms of host defense against influenza and mycobacterium tuberculosis.
2. Unravelling the mechanisms by which PAMPs and eicosanoids regulate the macrophage death modality on T cell mediated autoimmunity.
3. Designing a new generation of vaccines using recombinant or deleted gene based organisms and/or in combination with host eiosanoids modulation.

Selected publications: 
Research areas: 
Infectious Diseases
Respiratory diseases
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