I mathematically model immune memory regulation and memory repertoire
shifts resulting from memory T-cell attrition.
More specifically, I mathematically examine how the memory CD8+ T-cell
repertoire changes due to infections. Following
normal infections, the creation of new memory T-cells results in
increased competition for survival signals, which in turn may
lead to passive attrition of existing memory. Furthermore, some
viral infections cause massive bystander attrition of memory
CD8+ T-cells early in infection; this attrition is then followed by
homeostatic proliferation of surviving memory cells, along
with some naive cells, to refill the memory compartment. My work
looks at how these attrition events alter the composition of
lineages within the memory CD8+ T-cell repertoire and hence affect the
ability of the memory compartment to respond to
particular infections should they reoccur.