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Marcello Pinti

Researcher at University of Modena and Reggio Emilia

Publications -  185
Citations -  13448

Marcello Pinti is an academic researcher from University of Modena and Reggio Emilia. The author has contributed to research in topics: Mitochondrion & Immune system. The author has an hindex of 46, co-authored 163 publications receiving 11592 citations. Previous affiliations of Marcello Pinti include University of Milan & National Institutes of Health.

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Development of real time PCR assays for the quantification of Fas and FasL mRNA levels in lymphocytes: studies on centenarians.

TL;DR: The preliminary results suggest that during aging a subtle balance in the production of molecules that cause apoptosis could exist, and that, in order to avoid an excessive death of immune cells, a still unknown mechanism could compensate the increase of Fas with the reduction of FasL.
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Mitochondrial functionality and metabolism in T cells from progressive multiple sclerosis patients

TL;DR: The data suggest that profound differences exist in the phenotypic and metabolic features of T cells from PP and SP patients, even though the two clinical phenotypes are considered part of the same disease spectrum.
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Identification and characterization of an aspartyl protease from Cryptococcus neoformans.

TL;DR: The absence of any inhibition activity by PIs suggests that other targets for PIs might exist in C. neoformans, and identifies the gene cnap1, which codifies for a protein of 505 aa, with a canonical aspartyl protease structure.
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Mitochondrial DNA: a proinflammatory ‘enemy from within' during HIV infection?

TL;DR: The presence of significant amounts of DAMPs of mitochondrial origin in the peripheral blood of subjects with HIV infection suggests that part of the inflammation typical of such infection could be because of the activity of these molecules, and thus opens new therapeutic perspectives.
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CD4+ T-cell differentiation, regulatory T cells and gag-specific T lymphocytes are unaffected by CD4-guided treatment interruption and therapy resumption.

TL;DR: Treatment interruption resulted in a CD4+ cell count decrease and plasma viral load increase, but did not preclude a good immune reconstitution and a complete suppression of pVL after treatment resumption, and, on the contrary, could induce HIV-specific responses.