About me

Hi, I’m Danny.

I am an applied mathematician intersted in applications of maths to biology an immunology. My background is in pure maths, specifically abstract algebra and algebraic geometry, and my current work is based on deterministic and stochastic modelling of biological systems, using both mathematical and computational tools.

Current work

I am currently a research associate at the mathematical and theoretical immunology group in the Department of Infectious Disease led by Becca Asquith at Imperial College London. My current research is focussed on deterministic data driven models to understand the dynamics of specific understudied cell populations, in particular γδ T cells.

The main aim of my research is to model celullar proliferation dynamics, both on a single-cell level and a cell-population level, in order to provide estimates of per-cell proliferation rates.

PhD project

I completed my PhD in Applied Mathematics, specifically Mathematical Immunology, at the University of Leeds. I was part of the mathematical biology and medicine group and here is a short description of my project:

A T cell receptor can recognise a set of peptides presented by MHC, these can be foreign which cause an immune response, or the can be produced by the body itself which provide T cells with survival stimulus and cause them to divide. When considering several clonotype these sets of peptides can overlap, this is called cross-reactivity and it can be seen in the form of one infection causing immunity to more than one pathogen.

The aim of my project was to use stochastic models to study how cross-reactivity of self peptides influences the populations of clonotypes that compete for survival stimulus. The second aim of the project is to use a stochastic model of T cell clonotypes during infection to study the effects of cross-reactivity on the initial immune response, and subsequent memory responses. A second part of this is to study how clonal expansion during the immune response perturbs the distribution of clonal sizes after contraction back to homeostasis.