Person
TABELLINI Giovanna
Docenti di ruolo di IIa fascia
Course Catalogue:
Communications
Curriculum Vitae
Doctor Giovanna Tabellini was born in Portogruaro on the 20th December 1970.
In July 1997 she obtained a degree in Biological Science in the Faculty of Natural Sciences in the State University of Trieste. In 2005 she had Researcher place in Histology Unit of Faculty of Medicine of Brescia (Italy). Since 2005 she works in the research group of Prof. Silvia Parolini. She collaborates with the research group of Prof. Alessandro Moretta of DIMES (Department of Experimental Medicine) of University of Genoa (Italy). In his laboratory she had the possibility to specialize in the techniques of generation of monoclonal antibodies and cloning of human natural Killer lymphocytes.
In July 1997 she obtained a degree in Biological Science in the Faculty of Natural Sciences in the State University of Trieste. In 2005 she had Researcher place in Histology Unit of Faculty of Medicine of Brescia (Italy). Since 2005 she works in the research group of Prof. Silvia Parolini. She collaborates with the research group of Prof. Alessandro Moretta of DIMES (Department of Experimental Medicine) of University of Genoa (Italy). In his laboratory she had the possibility to specialize in the techniques of generation of monoclonal antibodies and cloning of human natural Killer lymphocytes.
Fields (8)
Free text keywords
LINFOCITI NATURAL KILLER UMANI, IMMUNITÀ INNATA, IMMUNODEFICIENZE, CARCINOMA OVARICO
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Research fields
Functional and expression analysis of new receptor molecules of human natural killer lymphocytes identified for the first time through the generation of monoclonal antibodies.
Functional analysis of Natural Killer cells in patients with various primary immunodeficiencies: in particular, patients suffering from:
- Hermansky-Pudlak type 2 syndrome,
- Wiskott-Aldrich syndrome (WAS) and WASP mutation
- mutations of WIP (WASP interacting protein)
- Pallidin protein mutations
- mutations of Dock2 and Dock8 protein
- mutations of NFKB2, NFKB1
- defects of STAT1,
- mutations of PI3Ks (p85alfa)
- mutations of RAG 1 and 2 (Recombinase-Activating Gene) and NHEJ proteins.
- studies are ongoing in patients with severe immune disorders that include severe functional deficits of NK cells caused by mutations of molecules with an important role in the immune response (IKKa, RAC2, CTLA-4) and by unknown diseases and / or unknown genetic defects.
Study of the role of human Natural Killer cells in the early phases of the immune response. Analysis of NK cell subsets from the peripheral blood and from secondary lymphoid tissues by cytofluorimetric, immunohistochemical and immunofluorescence analysis.
Since 2016 we has been collaborating with the Innate Pharma S.A. Company / Biopharmaceutical Company, Marseille, France, which has expertise in the production of immunotherapeutic drugs for tumors and inflammatory diseases.
Role of Natural Killer lymphocytes in patients with ovarian cancer. In recent years our research has focused on the functional mechanisms used by Natural Killer cells to recognize ovarian cancer cells. Epithelial ovarian cancer is the gynecological tumor with the highest mortality rate due to a high resistance to conventional therapies. In particular, the activating and inhibitory lymphocyte receptors were able to recognize expressed ligands, specifically from the autologous primary lines isolated from patients affected by ovarian cancer. We have identified some ligands that could be the cause of downregulation of activating receptors fundamental for the cytotoxic function of Natural Killer cells (B7 / H6, ligand of NKP30, and PRV and Nectin-2 ligands of DNAM-1) and ligands that would stimulate inhibitory receptors (PDL1 / 2 PD-1 ligands) expressed by certain histotypes of ovarian carcinoma.
Such inhibitory receptors can prevent and block anti-tumor activity. Recently, in collaboration with the research group led by Prof. A. Moretta (DIMES, University of Genoa) we have identified a small subset of NK cells of peripheral blood of healthy donors that expresses the PD-1 inhibitor receptor (Programmed Death Receptor 1).
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