Paolo Puccetti

TL;DR: A metabolic pathway whereby Trp metabolites from the microbiota balance mucosal reactivity in mice is described, whereby highly adaptive lactobacilli are expanded and produce an aryl hydrocarbon receptor (AhR) ligand-indole-3-aldehyde-that contributes to AhR-dependent Il22 transcription.

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.