Bio

I am both trained as a biomedical researcher and medical doctor in internal medicine and strive to close the gap between the clinic and fundamental sciences with translational research. My focus is to study the mechanisms of autoimmune diseases and to translate research insights into therapeutics targeting autoimmunity. I have received my PhD in 2022 in Leiden for studying neutrophil extracellular traps and autoreactive B cells in renal autoimmune diseases. My postdoctoral research project in the Robinson lab focuses on investigating the underlying molecular mechanisms of the pathogenesis of ANCA-associated vasculitis. I particularly aim to identify potential microbial triggers and molecular mimicry in ANCA-associated vasculitis, by characterizing the nasal microbiome and sequencing T cells and B cells of ANCA-associated vasculitis patients.

Honors & Awards

  • Marie Curie Fellowship, European Union (2024)
  • Selected for the best 30 abstracts, ERA-EDTA (2018)
  • Full travel grant NVVI, Dutch Federation of Immunology (NVVI) (2018)
  • Second prize in best abstract and oral presentation, Dutch Federation of Nephrology (NFN) Benelux Kidney Meeting (2019)
  • Kidney Star award recipient, American Society of Nephrology (ASN) (2019)

Professional Education

  • PhD, Leiden University Medical Center Department of Nephrology, “Targeting autoimmunity in renal diseases: focus on neutrophil extracellular traps and autoreactive B-cells” (2022)
  • MSc, University of Utrecht - Selective Utrecht Medical Master (SUMMA), Clinical Research (2016)
  • MD, University of Utrecht - Selective Utrecht Medical Master (SUMMA), Medicine (2016)
  • BSc, University of Amsterdam, Biomedical Sciences (2011)

Stanford Advisors

Contact

  • Academic
    lsvandam@stanford.edu
    University - Scholar Department: School of Medicine Position: Postdoctoral Scholar

Additional Info

Lab Affiliations

All Publications

  • Identification of Autoreactive Cytotoxic T Cells in ANCA-Associated Vasculitis van Dam, L., Younis, S., Moon, J., Zhang, M., Parfasar, S., Horomanski, A., Sharpe, O., van Leeuwen, J., Lanz, T., van Kooten, C., Teng, O., Robinson, W. WILEY. 2024: 3781-3785

    View details for Web of Science ID 001331419105286

  • Deficiency of Nuclear Receptor Nur77 Aggravates Mouse Experimental Colitis by Increased NFkB Activity in Macrophages PLOS ONE Hamers, A. J., van Dam, L., Duarte, J., Vos, M., Marinkovic, G., van Tiel, C. M., Meijer, S. L., van Stalborch, A., Huveneers, S., Velde, A., de Jonge, W. J., de Vries, C. M. 2015; 10 (8): e0133598

    Abstract

    Nuclear receptor Nur77, also referred to as NR4A1 or TR3, plays an important role in innate and adaptive immunity. Nur77 is crucial in regulating the T helper 1/regulatory T-cell balance, is expressed in macrophages and drives M2 macrophage polarization. In this study we aimed to define the function of Nur77 in inflammatory bowel disease. In wild-type and Nur77-/- mice, colitis development was studied in dextran sodium sulphate (DSS)- and 2,4,6-trinitrobenzene sulfonic acid (TNBS)-induced models. To understand the underlying mechanism, Nur77 was overexpressed in macrophages and gut epithelial cells. Nur77 protein is expressed in colon tissues from Crohn's disease and Ulcerative colitis patients and colons from colitic mice in inflammatory cells and epithelium. In both mouse colitis models inflammation was increased in Nur77-/- mice. A higher neutrophil influx and enhanced IL-6, MCP-1 and KC production was observed in Nur77-deficient colons after DSS-treatment. TNBS-induced influx of T-cells and inflammatory monocytes into the colon was higher in Nur77-/- mice, along with increased expression of MCP-1, TNFα and IL-6, and decreased Foxp3 RNA expression, compared to wild-type mice. Overexpression of Nur77 in lipopolysaccharide activated RAW macrophages resulted in up-regulated IL-10 and downregulated TNFα, MIF-1 and MCP-1 mRNA expression through NFκB repression. Nur77 also strongly decreased expression of MCP-1, CXCL1, IL-8, MIP-1α and TNFα in gut epithelial Caco-2 cells. Nur77 overexpression suppresses the inflammatory status of both macrophages and gut epithelial cells and together with the in vivo mouse data this supports that Nur77 has a protective function in experimental colitis. These findings may have implications for development of novel targeted treatment strategies regarding inflammatory bowel disease and other inflammatory diseases.

    View details for DOI 10.1371/journal.pone.0133598

    View details for Web of Science ID 000358942700017

    View details for PubMedID 26241646

    View details for PubMedCentralID PMC4524678

https://orcid.org/0000-0001-6373-7673