Honors & Awards

  • DAAD Graduate School Scholarship, DAAD (02/2017 - 02/2021)
  • Fulbright USA-Polish Commission Award, Fulbright (07/2015 - 07/2016)
  • Academic Achievement Scholarship, University of Wrocław (10/2014 - 07/2015)
  • Academic Achievement Scholarship, University of Wrocław (10/2011 - 07/2012)
  • LLP-Erasmus Placement Funding, Erasmus (10/2013 - 05/2014)
  • 5x Incentive scholarships for the bests students, EU (03/2011 - 07/2013)
  • First prize for the most active Bio-Scientific Student Association, University of Wroclaw (2013)

Professional Education

  • Doctor of Philosophy, Freie Universitat Berlin (2021)
  • Dr. rer. nat., Free University of Berlin, Cancer Immunology (2021)
  • M.Sc., University of Wrocław, Medical Biotechnology (2016)
  • B.Sc., University of Wrocław, Biotechnology (2013)

Stanford Advisors

Patents

  • Natalia Plewa, Lucia Poncette, Thomas Blankenstein. "Germany Patent EP4223782A1 Novel T cell Receptors and immune therapy for the treatment of cancer", Max-Delbrück-Centrum für Molekulare Medizin in der Helmholtz-Gemeinschaft, Charité - Universitätsmedizin Berlin

Contact

  • Academic
    nplewa@stanford.edu
    University - Scholar Department: Stanford Cancer Institute Core Position: Postdoctoral Scholar

Additional Info

  • Mail Code: 5458

Links

All Publications

  • Generation of TGFβR2(-1) neoantigen-specific HLA-DR4-restricted T cell receptors for cancer therapy. Journal for immunotherapy of cancer Plewa, N., Poncette, L., Blankenstein, T. 2023; 11 (2)

    Abstract

    Adoptive transfer of patient's T cells, engineered to express a T cell receptor (TCR) with defined novel antigen specificity, is a convenient form of cancer therapy. In most cases, major histocompatibility complex (MHC) I-restricted TCRs are expressed in CD8+ T cells and the development of CD4+ T cells engineered to express an MHC II-restricted TCR lacks behind. Critical is the choice of the target antigen, whether the epitope is efficiently processed and binds with high affinity to MHC molecules. A mutation in the transforming growth factor β receptor 2 (TGFβR2(-1)) gene creates a frameshift peptide caused by the deletion of one adenine (-1) within a microsatellite sequence. This somatic mutation is recurrent in microsatellite instable colorectal and gastric cancers and, therefore, is a truly tumor-specific antigen detected in many patients.ABabDR4 mice, which express a diverse human TCR repertoire restricted to human MHC II molecule HLA-DRA/DRB1*0401 (HLA-DR4), were immunized with the TGFβR2(-1) peptide and TGFβR2(-1)-specific TCRs were isolated from responding CD4+ T cells. The TGFβR2(-1)-specific TCRs were expressed in human CD4+ T cells and their potency and safety profile were assessed by co-cultures and other functional assays.We demonstrated that TGFβR2(-1) neoantigen is immunogenic and elicited CD4+ T cell responses in ABabDR4 mice. When expressed in human CD4+ T cells, the HLA-DR4 restricted TGFβR2(-1)-specific TCRs induced IFNy expression at low TGFβR2(-1) peptide amounts. The TGFβR2(-1)-specific TCRs recognized HLA-DR4+ lymphoblastoid cells, which endogenously processed and presented the neoantigen, and colorectal cancer cell lines SW48 and HCT116 naturally expressing the TGFβR2(-1) mutation. No MHC II alloreactivity or cross-reactivity to peptides with a similar TCR-recognition motif were observed, indicating the safety of the TCRs.The data suggest that HLA-DR4-restricted TCRs specific for the TGFβR2(-1) recurrent neoantigen can be valuable candidates for adoptive T cell therapy of a sizeable number of patients with cancer.

    View details for DOI 10.1136/jitc-2022-006001

    View details for PubMedID 36822673

    View details for PubMedCentralID PMC9950979

  • Rapid rerouting of myosin traffic at the T cell immunological synapse. Biophysical Journal Plewa, N., Maka, R., Cichon, U., Krysztofiak, K., Rokicka, J., Rock, R. 2022; 121 (3)

    View details for DOI 10.1016/j.bpj.2021.11.1434

  • Loss of Gadkin Affects Dendritic Cell Migration In Vitro. PloS one Schachtner, H., Weimershaus, M., Stache, V., Plewa, N., Legler, D. F., Höpken, U. E., Maritzen, T. 2015; 10 (12): e0143883

    Abstract

    Migration is crucial for the function of dendritic cells (DCs), which act as outposts of the immune system. Upon detection of pathogens, skin- and mucosa-resident DCs migrate to secondary lymphoid organs where they activate T cells. DC motility relies critically on the actin cytoskeleton, which is regulated by the actin-related protein 2/3 (ARP2/3) complex, a nucleator of branched actin networks. Consequently, loss of ARP2/3 stimulators and upstream Rho family GTPases dramatically impairs DC migration. However, nothing is known yet about the relevance of ARP2/3 inhibitors for DC migration. We previously demonstrated that the AP-1-associated adaptor protein Gadkin inhibits ARP2/3 by sequestering it on intracellular vesicles. Consistent with a role of Gadkin in DC physiology, we here report Gadkin expression in bone marrow-derived DCs and show that its protein level and posttranslational modification are regulated upon LPS-induced DC maturation. DCs derived from Gadkin-deficient mice were normal with regards to differentiation and maturation, but displayed increased actin polymerization. While the actin-dependent processes of macropinocytosis and cell spreading were not affected, loss of Gadkin significantly impaired DC migration in vitro, however, in vivo DC migration was unperturbed suggesting the presence of compensatory mechanisms.

    View details for DOI 10.1371/journal.pone.0143883

    View details for PubMedID 26624014

    View details for PubMedCentralID PMC4666629