CTLA-4–Ig regulates tryptophan catabolism in vivo
作者： Ursula Grohmann , Ciriana Orabona , Francesca Fallarino , Carmine Vacca , Filippo Calcinaro
DOI: 10.1038/NI846
关键词: Cytotoxic T cell 、 Immune tolerance 、 Intracellular 、 Transplantation 、 Fusion protein 、 Biology 、 In vivo 、 Biochemistry 、 Peripheral tolerance 、 Receptor
摘要: Cytotoxic T lymphocyte-associated antigen 4 (CTLA-4) plays a critical role in peripheral tolerance. However, regulatory pathways initiated by the interactions of CTLA-4 with B7 counterligands expressed on antigen-presenting cells are not completely understood. We show here that long-term survival pancreatic islet allografts induced soluble fusion protein CTLA-4-immunoglobulin (CTLA-4-Ig) is contingent upon effective tryptophan catabolism host. In vitro, we CTLA-4-Ig regulates cytokine-dependent B7-expressing dendritic cells. These data suggest modulation means which functions vivo and acts as ligand for receptor molecules transduce intracellular signals.
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