Damien John Zanker has completed his Bachelor of Science (Hons) degree in Physiology at the University of Melbourne studying therapeutic treatments of Retinopathy of Prematurity. In 2005, he began Research at the Ludwig Institute for Cancer Research at the Austin Hospital before undertaking a PhD through the University of Melbourne in 2008. His studies involved assessing the contribution of the immunoproteasome to generate peptides for immune responses as well as identifying novel non immune roles for this highly specialized type of proteasome. He is a Member of the NHMRC Influenza Program and currently researches CD8+ T cell immunity at La Trobe University, Australia.


Neutralizing antibodies are highly specific for a particular antigen. Viruses such as Influenza-A is commonly mutant to render strain specific neutralizing antibodies non functional against future infecting strains. Because of this, current antibody based influenza vaccines require reformulation annually. However, antigenic peptides that stimulate CD8+ T cell responses commonly arise from internal proteins that rarely mutate from antigenic drift. Due to this, memory CD8+ T cells are thought to be the most promising candidate to target for a cross strain universal influenza vaccine. The residential memory T-cell subset (TRM) is proposed as the frontline defense against pathogen re-encounter as previous studies have demonstrated this subset does not leave its tissue. Using a prime boost protocol, we wished to discover novel ways to enhance TRM numbers at the infection site in mice. Counter intuitively, we identified that initially priming an alternate site and boosting at the desired site dramatically enhanced the responding and memory T-cell pool in the lung. Using this alternate immunization technique, we also showed that peripheral effector memory T-cells were capable of transforming into lung TRM. This led us to believe that only particular antigen presenting cells were capable of inducing TRM formation. We also discovered that TRM formation was productive infection dependent and was required to protect against lethal re-infection. Together, by circumventing primary TRM formation, we were able to boost TRM at a desired site by an alternate immunization site strategy and believe this is an effective method to enhance TRM formation in the absence of adjuvant administration.