Immunotherapy toxicity is mediated by the activity of T lymphocyte clones that are driven by specific antigenic targets. In this project the student will use mouse and human samples to identify candidate T cell antigens that drive these maladaptive immune responses. These results will determine how changes in transcription caused by immunotherapy can change the display of antigen, and the potential this has for triggering tissue-damaging T cell responses.

Doctoral Training Partnerships: a range of postgraduate training is funded by the Research Councils. For information on current funding routes, see the common terminology at https://www.ukri.org/apply-for-funding/how-we-fund-studentships/. Training grants may be to one organisation or to a consortia of research organisations. This portal will show the lead organisation only.

Deciding whether or not to reach a target, or choosing which target to reach in the presence of multiple alternatives, require additional layers of cognitive control over spatiomotor transformations. These types of decisions are not simply driven by perceptual features of the target but also by our (possibly learned) expectations of what will happen once the target is reached. Moreover, in order to be effective, this level of cognitive control must operate in the same spatial reference frame as the action selection mechanisms that it oversees. In this project, the candidate will build on our previous work on the superior colliculus to assess the role of genetically defined collicular neurons as well as the extended cortical-collicular circuits in distinct aspects of cognitive control, from value allocation to decision making in space. The candidate will use cutting-edge methods to map and manipulate neural circuits in vivo and leverage non the novel behavioural assays and recording methods developed in the lab.

Individuals with Intellectual Disability of known genetic origin show differences in behavioural characteristics depending on the membership of their gene variant to a group with convergent cellular mechanisms, referred to as a Gene Functional Network (GFN). However, the relationships between GFNs and brain organisation are yet to be explored. I propose using network analyses to examine whether genetic cause, classified by GFN membership, is associated with differences in organisational principles of behaviour, brain function and brain structure. Two GFNs will be examined: those that are direct and indirect modifiers of synaptic physiology, and those that are chromatin structure modifiers.

During my PhD, I would like to investigate phantom limb pain (PLP), a chronic pain syndrome that occurs after amputation, and affects the majority of amputees. The research project involves three studies, which would explore both peripheral and central contributions to PLP, and be the first set of studies to look at the relationship between peripheral signals and how they are exasperated by cognitive mechanisms. For the first study, I would use TMS combined with EMG to elicit phantom hand sensations, which have been shown to be one of the most common factors positively associated with PLP. This would aid our understanding of the shared mechanisms and potential mechanistic association to PLP. The second study would focus on how cognitive biases in pain learning relate to PLP, building on computational models from reinforcement learning to see how people gather peripheral evidence. Using thermal stimulation to deliver stimuli and recording EMG activity during phantom movements, I will gather empirical evidence to explore amputees' expectations of pain and experienced pain. The third study will aim to causally test the models built in the first study by seeing the effect of a novel surgical procedure that reduces PLP - targeted muscle reinnervation (TMR). By conducting a within-subjects experiment, testing before and after the procedure, we can additionally provide objective evidence on TMR reducing the processing of pain.