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Francesco Bistoni

Researcher at University of Perugia

Publications -  340
Citations -  18620

Francesco Bistoni is an academic researcher from University of Perugia. The author has contributed to research in topics: Candida albicans & Immune system. The author has an hindex of 74, co-authored 340 publications receiving 17890 citations. Previous affiliations of Francesco Bistoni include Yeshiva University & Sigma-Tau.

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Immortalization of murine microglial cells by a v-raf / v-myc carrying retrovirus

TL;DR: Since BV-2 cells retain most of the morphological, phenotypical and functional properties described for freshly isolated microglial cells, it can be concluded that J2 virus infection has resulted in the immortalization of active microglia cells.
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IL-23 and the Th17 pathway promote inflammation and impair antifungal immune resistance.

TL;DR: The data are the first demonstrating that the IL‐23/IL‐17 pathway promotes inflammation and susceptibility in an infectious disease model and modulation of the inflammatory response represents a potential strategy to stimulate protective immune responses to fungi.
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Defective tryptophan catabolism underlies inflammation in mouse chronic granulomatous disease

TL;DR: It is shown that a superoxide-dependent step in tryptophan metabolism along the kynurenine pathway is blocked in CGD mice with lethal pulmonary aspergillosis, leading to unrestrained Vγ1+ γδ T-cell reactivity, dominant production of interleukin (IL)-17, defective regulatory T- cell activity and acute inflammatory lung injury.
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Reverse signaling through GITR ligand enables dexamethasone to activate IDO in allergy.

TL;DR: It is shown that reverse signaling through GITRL after engagement by soluble GITR initiates the immunoregulatory pathway of tryptophan catabolism in mouse plasmacytoid dendritic cells, by means of noncanonical NF-κB–dependent induction of indoleamine 2,3-dioxygenase (IDO).
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Impaired neutrophil response and CD4+ T helper cell 1 development in interleukin 6-deficient mice infected with Candida albicans.

TL;DR: In this paper, the role of interleukin (IL)6 in Candida albicans infection was defined and IL-6 deficient mice were assessed for susceptibility to systemic or gastrointestinal infection, as well as for parameters of elicited T helper cell immunity.