Before a disease can be treated, it must first be understood. That means pinpointing its extrinsic environmental components, which include exposure to such risk factors as diet and lifestyle, and its intrinsic factors, which comprise the complex interaction of genetic factors. With the help of powerful bioinformatics tools, scientists in the McGill University Research Centre on Complex Traits (MRCCT) in McGill鈥檚 Life Sciences Complex examine the interplay between these components. Their findings are leading to the identification of new pathways, genes and proteins involved in the onset, progression and, ultimately, the outcome of a disease. This provides a foundation on which new tools for better prevention and treatment of these conditions can be developed.

"The Life Sciences Complex has enabled a diverse group of researchers that includes biochemists, geneticists, microbiologists, immunologists, physiologists and computational biologists with a unique opportunity to work side by side," says Dr. Silvia Vidal, Professor of Human Genetics and Director of the MRCCT. "The quality of the research and animal facilities accelerated the recruitment of top talented young investigators and trainees. This setting has allowed us to launch ambitious collaborative projects that have characterized the genetic basis of host susceptibility to infection and identified new genes and mechanisms in mouse models of human infectious diseases, some of which are currently being explored for their potential applications to treat not only severe infections but also inflammatory diseases."

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Three big breakthroughs in Complex Traits

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1.Halting cell death to save the host: Assistant Professor in Microbiology and Immunology Dr. Maya Saleh's research aims to shed light on cell death pathways and the link between cell death and inflammation. In the past, it was thought that all the damage wrought by an infectious disease was caused by the pathogen that arrives and kills the cells. But now we realize that a lot of the damage is caused by overreactive responses in the immune system. Dr. Saleh and her lab are working to understand this interplay between innate immune response, cell death and inflammation, with the hope that it will open up new approaches to therapeutics for diseases as diverse as cancer, inflammatory bowel disease and influenza.

Cell Host and Microbe. 1

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2. Rare cell type displays flu-busting potential: Dr. J枚rg Fritz, Associate Professor in Microbiology and Immunology, characterized a new cell type in mice lungs called type 2 innate lymphoid cells (ILC2s). Though rare, these cells can teach us important lessons about how they develop and how they modify their immune responses to influenza. ILC2s appear to help maintain airway barrier integrity and lung tissue homeostasis after viral infections. Apart from these protective qualities, ILC2s can also trigger deregulated immune responses, which can worsen an infection. A better understanding of both kinds of ILC2 responses can pinpoint possible preventative and therapeutic routes for respiratory infections, which carry a huge disease burden worldwide.

Nature Immunology. 2016 Jan;17(1):65-75. doi: 10.1038/ni.3308. Epub 2015 Nov 23. Type I interferon restricts type 2 immunopathology through the regulation of group 2 innate lymphoid cells.

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3. Cysteamine for drug-resistant malaria: Professor of Biochemistry Dr. Philippe Gros and his team have been studying the response of mice infected with Plasmodium falciparum, the parasite that causes cerebral malaria, to the drug cysteamine (approved for treatment of the kidney disorder nephropathic cystinosis). Its promising use as an adjuvant for the anti-malarial drug artemisinin (to which the malaria parasite has developed resistance) is now being studied in clinical trials. As an added bonus, when used in combination with cysteamine, artemisinins can be administered in lower doses. This discovery has the potential to influence millions of people, in particular children who are the most affected by malaria.

Malaria Journal.2016 May 6;15(1):260. doi: .