Dr. Martin Allan
During his PhD, Allan worked on the kinetics of T cell responses. The first aim of Martin’s project was to identify the most plausible mechanism that could regulate the T cell kinetics during an acute response. Using an ODE compartmental model to keep track of the number of cells in each generation, he compared the predictions of a number of plausible regulatory mechanisms to experimental data to determine the potential of each to regulate cell number.
One revealing conclusion of his work was that all successful mechanisms progressively increase the apoptosis rate during the response. He then assessed the most plausible mechanisms and then determined which produced the least wasteful response (in terms of unnecessary T cell death). He concluded that the most plausible mechanism is one that progressively increases death rates and decreases division rates.
The second aim of this project was to investigate how the programmed nature of the regulatory mechanism affected the outcome of infection. He considered two aspects of the outcome of infection: the size of the generated memory population, and the success, or otherwise, of pathogen clearance. Martin extended the previous compartmental model to incorporate the formation of memory cells, and established the impact of the program parameters on the final memory size following an acute infection. He considered situations when the pathogen can persist beyond the acute phase, and he developed a discrete-time population model to predict the long-term behaviour of the response. He found that if the developmental program always produces a net increase in cell population size then pathogen clearance is guaranteed. A further conclusion of his work was that during this long-term infection the sensitivity of the specific memory cells to re-stimulation diminishes.
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