Tracy L. McGaha

Dr. McGaha obtained his Ph.D. in Immunology at the Ichan School of Medicine at New York University in 2002, and pursued post-doctoral training at the Rockefeller University from 2002 to 2006. Dr. McGaha joined the Princess Margaret Cancer Centre as a Senior Scientist in 2015. He is also an Associate Professor in the Department of Immunology at the University of Toronto. Dr. McGaha has a research interest that encompasses the cell communication and immune-suppressive mechanisms in the occurrence of apoptosis; his laboratory uses an in vivo model of apoptotic cell challenge testing potential mechanism involved in the innate response elicited by tissue-resident macrophages and dendritic cells. In particular they are interested in apoptotic cell-driven chemotaxis and functional interactions between tissue resident macrophages, tolerogenic CD103+ dendritic cells and regulatory T cell populations. The McGaha Lab was one of the first to demonstrate that specialized tissue-resident stromal macrophages control early immunity to apoptotic cells regulating both dendritic cell and T cell responses to apoptotic antigens, and disrupting the function of these macrophage subsets renders mice susceptible to apoptotic cell-driven autoimmune disease. In juxtaposition, the team is also studying how immune responses to programmed cell death are influenced by the metabolic stress signals and innate signaling, in the context of autoimmunity and cancer.

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Princess Margaret Cancer Centre, University Health Network

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Autoimmunity 0 Immune Suppressive Mechanisms 0 Apoptosis 0

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  2. Halaby MJ, Hezaveh K, Lamorte S, et al. GCN2 drives macrophage and MDSC function and immunosuppression in the tumor microenvironment. Sci Immunol. 2019;4(42):eaax8189.

  3. Gadalla R, Noamani B, MacLeod BL, et al. Validation of CyTOF Against Flow Cytometry for Immunological Studies and Monitoring of Human Cancer Clinical Trials. Front Oncol. 2019;9:415. Published 2019 May 17.

  4. Roux C, Jafari SM, Shinde R, et al. Reactive oxygen species modulate macrophage immunosuppressive phenotype through the up-regulation of PD-L1. Proc Natl Acad Sci U S A. 2019;116(10):4326-4335.

  5. Shinde R, Hezaveh K, Halaby MJ, et al. Apoptotic cell-induced AhR activity is required for immunological tolerance and suppression of systemic lupus erythematosus in mice and humans. Nat Immunol. 2018;19(6):571-582.


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