Dunn School of Pathology University of Oxford

A wide range of chronic degenerative diseases of mankind result from the accumulation of altered forms of self proteins, resulting in cell toxicity, tissue destruction and chronic inflammatory processes in which the body’s immune system contributes to further cell death and loss of function. A hallmark of these conditions, which include major disease burdens such as Alzheimer’s Disease and type II diabetes, is the formation of long fibrillar polymers that are deposited in expanding tangled masses called plaques. Recently, similarities between these pathological accumulations and physiological mechanisms for organising intracellular space have been recognised, and formal demonstrations that amyloid accumulations form hydrogels have confirmed this link. We are interested in the pathological consequences of amyloid hydrogel formation and in order to study these processes we combine modelling of the assembly process with biophysical measurement of gelation and its cellular consequences.

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T cells stimulation by antigen (peptide-MHC, pMHC) initiates adaptive immunity, a major factor contributing to vertebrate fitness. The T cell antigen receptor (TCR) present on the surface of T cells is the critical sensor for the recognition of and response to “foreign" entities, including microbial pathogens and transformed cells. Much is known about the complex molecular machine physically connected to the TCR to initiate, propagate and regulate signals required for cellular activation. However, we largely ignore the physical distribution, dynamics and reaction energetics of this machine before and after TCR binding to pMHC. I will illustrate a few basic notions of TCR signalling and potent quantitative in-cell approaches used to interpret TCR signalling behaviour. I will provide two examples where mathematical formalisation will be welcome to better understand the TCR signalling process.

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