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Camilla Basso

Researcher at University of Lugano

Publications -  11
Citations -  1432

Camilla Basso is an academic researcher from University of Lugano. The author has contributed to research in topics: Colorectal cancer & Experimental autoimmune encephalomyelitis. The author has an hindex of 6, co-authored 8 publications receiving 878 citations.

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L-Arginine Modulates T Cell Metabolism and Enhances Survival and Anti-tumor Activity.

TL;DR: Elevating L-arginine levels induced global metabolic changes including a shift from glycolysis to oxidative phosphorylation in activated T cells and promoted the generation of central memory-like cells endowed with higher survival capacity and, in a mouse model, anti-tumor activity.
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T‐cell trafficking in the central nervous system

TL;DR: How pathogenic T cells can enter into intact or inflamed central nervous system to cause experimental autoimmune encephalomyelitis or multiple sclerosis is described and the role of CCR6/CCL20 axis in migration through the choroid plexus is elaborate.
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Metabolic modulation of tumours with engineered bacteria for immunotherapy

TL;DR: An engineered probiotic Escherichia coli Nissle 1917 strain that colonizes tumors and continuously converts ammonia, a metabolic waste product that accumulates in tumors4, into L-arginine shows that engineered microbial therapies enable metabolic modulation of the tumor microenvironment leading to enhanced efficacy of immunotherapies.
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Experimental priming of encephalitogenic Th1/Th17 cells requires pertussis toxin-driven IL-1β production by myeloid cells

TL;DR: Light is shed on the enigmatic function of PTX in EAE induction and inflammatory monocytes and microbial infection can influence differentiation of pathogenic Th1/Th17 cells in autoimmune diseases through production of IL-1β.
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ERK phosphorylation and miR-181a expression modulate activation of human memory T H 17 cells

TL;DR: It is shown that miR-181a is selectively induced in both human and mouse naive T cells differentiating into the TH17, but not TH1 or TH2 subset, thus influencing memory responses.