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Tuna Mutis

Researcher at VU University Amsterdam

Publications -  183
Citations -  10283

Tuna Mutis is an academic researcher from VU University Amsterdam. The author has contributed to research in topics: Cytotoxic T cell & Antigen. The author has an hindex of 44, co-authored 174 publications receiving 8771 citations. Previous affiliations of Tuna Mutis include Utrecht University & University of Groningen.

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Daratumumab depletes CD38+ immune-regulatory cells, promotes T-cell expansion, and skews T-cell repertoire in multiple myeloma

TL;DR: Depletion of CD38(+) immunosuppressive cells, which is associated with an increase in T-helper cells, cytotoxic T cells, T-cell functional response, and TCR clonality, represents possible additional mechanisms of action for daratumumab and deserves further exploration.
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Hematopoiesis-restricted minor histocompatibility antigens HA-1- or HA-2-specific T cells can induce complete remissions of relapsed leukemia.

TL;DR: HA-1- and HA-2-specific cytotoxic T lymphocytes emerging in the blood of patients after DLI demonstrate graft-versus-leukemia or myeloma reactivity resulting in a durable remission, implying that in vitro generated HA- 1- and HLA-A2/HA-2 peptide tetrameric complexes could be used as adoptive immunotherapy to treat hematological malignances relapsing after alloSCT.
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Antibody-mediated phagocytosis contributes to the anti-tumor activity of the therapeutic antibody daratumumab in lymphoma and multiple myeloma

TL;DR: It is demonstrated that phagocytosis is a fast, potent and clinically relevant mechanism of action that may contribute to the therapeutic activity of DARA in multiple myeloma and potentially other hematological tumors.
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Regulation of Treg functionality by acetylation-mediated Foxp3 protein stabilization

TL;DR: Modulation of the acetylation state of Foxp3 provides a novel molecular mechanism for assuring rapid temporal control ofFoxp3 levels in T cells, thereby regulating Treg numbers and functionality and could provide a new therapeutic strategy to control inappropriate (auto)immune responses.