Nature Immunology4, 1206 - 1212 (2003)
Published online: 26 October 2003; | doi:10.1038/ni1003
Modulation of tryptophan catabolism by regulatory T cells
Francesca Fallarino1, Ursula Grohmann1, Kwang Woo Hwang2, Ciriana Orabona1, Carmine Vacca1, Roberta Bianchi1, Maria Laura Belladonna1, Maria Cristina Fioretti1, Maria-Luisa Alegre2
& Paolo Puccetti1
1
Department of Experimental Medicine, University of Perugia, 06126 Perugia, Italy.
2
Department of Medicine, University of Chicago, Chicago, Illinois 60637, USA.
Correspondence should be addressed to Paolo Puccetti plopcc@tin.it
Regulatory T (TR) cells manifest constitutive expression of cytotoxic T lymphocyte−associated antigen 4 (CTLA-4), but the function of CTLA-4 in mediating the regulatory function of TR cells is unclear. We show here 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 CTLA-4-dependent mechanism. This process required B7 expression and cytokine production by the dendritic cells. In contrast, TR cells cultured in the presence of bacterial lipopolysaccharide induced tryptophan catabolism by dendritic cells in a CTLA-4-independent but cytokine-dependent way. Thus, regulation of immunosuppressive tryptophan catabolism in dendritic cells might represent a major mechanism of action of TR cells.
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