Benjamin Thompson


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.



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.


  • Severe type I interferonopathy and unrestrained interferon signaling due to a homozygous germline mutation in STAT2.

    Duncan CJA, Thompson BJ et al.

    Science Immunology 2019, 4(42), eaav7501.

  • Delayed induction of type I and III interferons and nasal epithelial cell permissiveness to SARS-CoV-2

    Hatton CF, Botting RA, Dueñas ME, Haq IJ, Verdon B, Thompson BJ et al.

    Nature Communications 2021, 12(7092)

  • Variants in STXBP3 are Associated with Very Early Onset Inflammatory Bowel Disease, Bilateral Sensorineural Hearing Loss and Immune Dysregulation

    Ouahed J, Thompson BJ, et al.

    Journal of Crohn’s and Colitis 2021 15(11),

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