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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)

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Grohmann, U. et al.

Grohmann, Orabona, Fallarino, Vacca, Calcinaro, Falorni, Candeloro, Belladonna, Bianchi, Fioretti, Puccetti,

CTLA-4-Ig regulates tryptophan catabolism in vivo.

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 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. In vitro, we show that CTLA-4-Ig regulates cytokine-dependent tryptophan catabolism in B7-expressing dendritic cells. These data suggest that modulation of tryptophan catabolism is a means by which CTLA-4 functions in vivo and that CTLA-4 acts as a ligand for B7 receptor molecules that transduce intracellular signals.[1]

References

CTLA-4-Ig regulates tryptophan catabolism in vivo. Grohmann, U., Orabona, C., Fallarino, F., Vacca, C., Calcinaro, F., Falorni, A., Candeloro, P., Belladonna, M.L., Bianchi, R., Fioretti, M.C., Puccetti, P. Nat. Immunol. (2002) [Pubmed]

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