Roberta Bianchi

TL;DR: It is shown that mouse CD4+CD25+ cells, either resting or induced to overexpress CTLA-4 by treatment with antibody to CD3, initiated tryptophan catabolism in dendritic cells through a CT LA-4-dependent mechanism, which might represent a major mechanism of action of TR cells.

TL;DR: It is shown that long-term survival of pancreatic islet allografts induced by the soluble fusion protein CTLA-4–immunoglobulin (CTLA- 4–Ig) is contingent upon effective tryptophan catabolism in the host and that CTla-4 acts as a ligand for B7 receptor molecules that transduce intracellular signals.

TL;DR: Evidence is provided that the short-term, combined effects of tryptophan deprivation and tryPTophan catabolites result in GCN2 kinase-dependent down-regulation of the TCR ζ-chain in murine CD8+ T cells.

TL;DR: It is shown that tryptophan metabolites in the kynurenine pathway, such as 3-hydroxyanthranilic and quinolinic acids, will induce the selective apoptosis in vitro of murine thymocytes and of Th1 but not Th2 cells, suggesting that the selective deletion of T lymphocytes may be a major mechanism whereby tryptophile metabolism affects immunity under physiopathologic conditions.

TL;DR: The Ca2+-binding protein of the EF-hand type, S100B, exerts both intracellular and extracellular functions, which might have important implications during brain, cartilage and skeletal muscle development and repair, activation of astrocytes in the course of brain damage and neurodegenerative processes, and of cardiomyocyte remodeling after infarction.