Benjamin Thompson

Research

Host cells infected with intracellular pathogens rely upon the recognition of non-self biomolecules, termed pathogen-associated molecular patterns (PAMPs), such as virally-derived nucleic acids. Cytoplasmic RNAs are sensed by members of the RIG-I-like receptor (RLR) family, ultimately cumulating in the expression of type I interferon (IFNα/β) cytokines and their potent downstream anti-viral properties. As such, the stringent regulation of type I IFN is paramount in maintaining healthy immune homeostasis. The type I interferonopathies are a broad category of monogenic inborn errors of immunity stemming from an inability to curtail type I IFN activity. Mutations within the RLR genes can results in the aberrant recognition of self-RNA molecules and sterile activation of anti-viral signalling. My research aims to examine multiple aspects of the biochemistry of nucleic acid sensing and regulation. Firstly, I will be investigating the nature of self-RNAs involved in aberrant RLR activation, and how this may relate to the well-described downstream consequences of dysregulated RNA-sensing. Secondly, I will be identifying and validating novel regulators of RNA sensing and type I IFN induction.

CURRICULUM VITAE

I obtained my Bachelor in Biomedical Sciences and Master of Research in Immunobiology from Newcastle University, United Kingdom in 2014 and 2015 respectively. In 2016, I was awarded a Medical Research Council grant to undertake a PhD at Newcastle University under the supervision of Professor Sophie Hambleton and Dr Christopher Duncan, investigating paediatric genetic lesions of autoinflammatory innate immunity with a particular interest in perturbations of type I interferon signalling. In April 2021 I moved to LUMC and began working with Dr Annemarthe van der Veen as a post-doctoral researcher.