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Leonardo Scarpellino

Researcher at University of Lausanne

Publications -  41
Citations -  3232

Leonardo Scarpellino is an academic researcher from University of Lausanne. The author has contributed to research in topics: Cytotoxic T cell & MHC class I. The author has an hindex of 24, co-authored 37 publications receiving 2671 citations. Previous affiliations of Leonardo Scarpellino include Ludwig Institute for Cancer Research & University of Verona.

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Intratumoral Tcf1+PD-1+CD8+ T Cells with Stem-like Properties Promote Tumor Control in Response to Vaccination and Checkpoint Blockade Immunotherapy.

TL;DR: This work identified a subset of tumor‐reactive TILs bearing hallmarks of exhausted cells and central memory cells, including expression of the checkpoint protein PD‐1 and the transcription factor Tcf1 that promote tumor control in response to vaccination and checkpoint blockade immunotherapy.
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Long-term, multilineage hematopoiesis occurs in the combined absence of beta-catenin and gamma-catenin

TL;DR: Ex vivo reporter gene assays provide the first evidence that hematopoietic cells can transduce canonical Wnt signals in the combined absence of beta- and gamma-catenin, and show that Wnt signal transmission is maintained in double-deficient hematoplastic stem cells, thymocytes, or peripheral T cells.
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Cis association of Ly49A with MHC class I restricts natural killer cell inhibition.

TL;DR: It is shown that the inhibitory Ly49A NK cell receptor not only binds to its H-2Dd ligand expressed on potential target cells but also is constitutively associated with H- 2Dd in cis (on the same cell).
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Superantigen-induced immune stimulation amplifies mouse mammary tumor virus infection and allows virus transmission

TL;DR: It is shown that transmission of an infectious MMTV is prevented when superantigen-reactive cells are absent through either clonal deletion due to the expression of an endogenous MTV with identicalsuperantigen specificity or exclusion due to expression of a transgenic TCR beta chain that does not interact with the viral superantigens.
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Sustained NKG2D engagement induces cross-tolerance of multiple distinct NK cell activation pathways

TL;DR: It is shown that receptors that activate NK cells via the DAP12/KARAP and DAP10 signaling adaptors, such as murine NKG2D and Ly49D, cross-tolerize preferentially NK cell activation pathways that function independent of DAP 10/12, suchAs antibody-dependent cell-mediated cytotoxicity and missing-self recognition.