Dr. Annemarthe van der Veen

Brief summary of research:

My team and I are interested in the innate immune mechanisms that control viral infection and sterile inflammation. I pursued my PhD with Hidde Ploegh at the Whitehead Institute at MIT. Here, I worked on ubiquitin-like proteins and studied their role in cellular homeostasis and stress responses. After my PhD, I joined the laboratory of Caetano Reis e Sousa at The London Research Institute and later on at The Francis Crick Institute in London to study the innate immune mechanisms that are important for antiviral immunity. I investigated how the activation of RNA sensors by viral RNA in the cytosol of infected cells controls the production of type I interferons, which are essential antiviral cytokines. In addition, I studied the role of RNA interference as an antiviral defense mechanism in mammals. During my time in the USA and the UK I was funded by the Boehringer Ingelheim Fonds, EMBO, and NWO Rubicon. In 2019, I joined the LUMC to continue my research. Thinking about viral ligands led to thinking about self-derived ligands. My team therefore studies how the RNA sensing pathway is activated by endogenous ligands, leading to innate immune activation in the absence of an infection. The consequent sterile inflammatory response contributes to autoinflammatory and autoimmune diseases and impacts on anti-tumor immunity and tumor rejection. Our work is funded by the Institute of Chemical Immunology and an LUMC fellowship.

 

Curriculum vitae

Current and previous positions:

2019-present   Assistant professor, Dept of Immunology, LUMC, the Netherlands

2015-2018       Post-doctoral fellow, The Francis Crick Institute (London, UK)

2011-2015       Post-doctoral fellow, The London Research Institute (London, UK)

 

Education:

2005-2011       PhD, Whitehead Institute for Biomedical Research (Cambridge, USA)

2003-2005       MSc, Biomedical Sciences, Utrecht University (NL)

2000-2003       BSc, University College Utrecht (NL)

 

Publications

  • RNA sensing via the RIG-I-like receptor LGP2 is essential for the induction of a type I IFN response in ADAR1 deficiency

    Stok JE*, Oosenbrug T*, Ter Haar LR, Gravekamp D, Bromley CP, Zelenay S, Reis e Sousa C, Van der Veen AG

    The EMBO Journal, Feb 14 2022, DOI: 10.15252/embj.2021109760

  • The RIG-I-like receptor LGP2 inhibits Dicer-dependent processing of long double-stranded RNA and blocks RNA interference in mammalian cells

    van der Veen AG, Maillard PV, Schmidt JM, Lee SA, Deddouche-Grass S, Borg A, Kjær S, Snijders AP, Reis e Sousa C.

    EMBO J. 2018 Feb 15;37(4). pii: e97479.

  • Inactivation of the type I interferon pathway reveals long double-stranded RNA-mediated RNA interference in mammalian cells

    Maillard PV, Van der Veen AG, Deddouche-Grass S, Rogers NC, Merits A, Reis e Sousa C.

    EMBO J. 2016 Dec 1;35(23):2505-2518.

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