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Three-dimensional rendering of an influenza-infected lung. T cells (red) contact the infected airway epithelium, which autofluoresces green.
Research - Technology Transfer - Focus Areas
Focus Areas


Traditional vaccines protect us from infection by eliciting pathogen-specific antibodies that circulate in the bloodstream. While these antibody-based vaccines have proven effective against a number of infectious diseases, they are ineffective or require repeated boosting when used to combat many others, including influenza, tuberculosis, herpes and plague. Trudeau’s first Director, Dr. George B. Mackaness, is widely credited with the discovery that another component of the immune system - the cellular immune response - provides an alternative means by which vaccination can combat infectious disease. It is now widely acknowledged that vaccines that stimulate cellular immunity offer tremendous promise. A number of Trudeau Institute scientists are striving to fulfill that promise. We have developed vaccine models of influenza, tuberculosis, bacterial pneumonia, herpes, plague, listeriosis, and toxoplasmosis in which cellular immunity confers mice with durable protection. Using these models, we are studying the mechanisms that regulate cellular immune responses and determining how to elicit potent, protective and durable cellular immunity.


Trudeau Institute’s faculty includes many specialists with expertise in pulmonary immunity. We study a number of pathogens that infect the lung and four of the world’s most deadly pulmonary diseases - influenza, tuberculosis, pneumonia and plague. Our many scientific contributions in this area have provided vast new information about how the immune system combats pulmonary infections. Now, we are using that knowledge to develop vaccines that selectively eradicate pulmonary pathogens without eliciting collateral pathology. Specifically, we are studying the cellular and humoral mechanisms used by immunity to combat pulmonary pathogens, and working to identify pathogen components that induce the most protective immunological memory. In parallel, we are working to develop therapeutic regimens that confer protection within moments of administration, thereby providing defense when infection has already occurred, or when exposure is suspected.


The complex mechanisms used by immunity to combat infection have evolved in humans over many millennia and are critical to surviving infectious disease. Unfortunately, they often go awry or become chronically activated. Then, the immune system's destructive power can cause serious disease. It is widely acknowledged that dysregulated immunity promotes inflammation, which in turn promotes vascular disease, asthma, anemia, sepsis, arthritis, diabetes, and multiple sclerosis. Our studies of the mechanisms dictating the development, migration, activation, and persistence of immune cells during infection often generate new information about how immunity is regulated, and how its dysregulation can initiate and perpetuate inflammation, autoimmunity and sepsis.


As individuals age, their ability to resist infection declines, in part due to changes in the immune system. The impact of age on the immune system also reduces vaccine efficacy in the elderly. Trudeau Institute scientists have developed models for studying the impact of age on immunity and for designing vaccines that better protect the elderly. By applying our infection models to our prized colonies of aged mice, Trudeau researchers discovered that aging is associated with a decline in the functional capacities of certain T cell subsets. Now we are working to overcome these age-related deficits. We have found that certain vaccine adjuvants can improve the functional capacity of aged T cells. This exciting observation indicates that it should be possible to develop vaccines that better protect the elderly from infection. Currently we are determining precisely how aging impairs T cell function, what initiates the impairment, and how certain adjuvants overcome the age-related deficits in immune function.

For additional information, please contact:

Atsuo Kuki, Ph.D.
President & Director

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