Mark Mensink

PhD student

Research

Immune responses depend on a dynamic balance between conventional (Tconv) and regulatory (Treg) T cells. Treg cells counteract the activity of conventional CD4 and CD8 T cells, thereby preventing excessive inflammation and autoimmunity. However, Treg cells can also constrain immune responses against tumors or chronic infections. Therefore, it is desired to specifically control Tconv or Treg cells for therapeutic purposes.

Many costimulatory receptors that have become clinical targets of antibody-based drugs are shared between Tconv and Treg cells. However, available data suggest that Treg cells have a differential wiring of signaling cascades downstream of such receptors. Using multi-omics approaches, we aim to identify key differences in costimulatory receptor signaling between Tconv and Treg cells, potentially allowing for selective drug targeting.

 

Curriculum vitae

I obtained my Master’s degree in Biomedical Sciences at the University of Amsterdam in 2016. During my studies, I performed a research internship in the laboratory of Professor Jacques Neefjes at the Netherlands Cancer Institute, where I investigated regulatory mechanisms of endosome positioning. My next internship was performed in the laboratory of Professor Suzanne Cory at the Walter and Eliza Hall Institute in Melbourne, where I studied resistance to apoptosis in Myc-driven B-cell lymphomas. In 2016, I started my PhD in the laboratory of Professor Jannie Borst at the Netherlands Cancer Institute. In 2019, our group moved to the LUMC to continue our research.

Publications

  • Stable human regulatory T cells switch to glycolysis upon TNF receptor 2 costimulation.

    de Kivit, S., Mensink, M., Hoekstra, A.T., Berlin, I., Derks, R.J.E., Both, D., Aslam, M.A., Amsen, D., Berkers, C.R., and Borst, J.

    Nat. Metab. 2: 1046-1061, 2020.

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