CTLA-4–Ig regulates tryptophan catabolism in vivo

By U. Grohmann, C. Orabona, Francesca Fallarino, C. Vacca, F. Calcinaro, A. Falorni, Paola Candeloro, M. L. Belladonna, R. Bianchi, M. Fioretti and 1 more. Nature Immunology, 2002

1,274 citations recorded by the source corpus.

Subfields: Genetics, Immunology

View Paper: https://www.semanticscholar.org/paper/9a04374a99a96ea8cf992e66451836a817bc28a2

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

In Genetics

1. D. Munn
2. A. Mellor
3. Shimon Sakaguchi
4. B. Fife
5. E. Shevach
6. Craig B. Thompson
7. J. Bluestone

In Immunology

1. D. Munn
2. Shimon Sakaguchi
3. A. Mellor
4. E. Shevach
5. V. Bronte
6. James P. Allison
7. J. Bluestone
8. T. Nomura

Citations in the corpus

• Foxp3+CD25+CD4+ natural regulatory T cells in dominant self‐tolerance and autoimmune disease (2006, background): “One is that CTLA-4 on Tregs may interact with the CD80/CD86 molecules on APCs and may transduce a costimulatory signal to Tregs, i.e. signals via CTLA-4 and TCR together may activate Tregs to exert suppression.”
• Plasmacytoid dendritic cells from mouse tumor-draining lymph nodes directly activate mature Tregs via indoleamine 2,3-dioxygenase. (2007, background): “2 molecules on DCs, resulting in B7-mediated induction of IDO (10, 28).”
• Mechanisms of foxp3+ T regulatory cell-mediated suppression. (2009, positive): “Human CD4+CD25+Foxp3+ Treg cells can be activated by a combination of antibodies to CD3 and CD46 to express granzyme A and kill activated CD4+ and CD8+ T cells and other cell types in a perforin-dependent, Fas-FasL-independent manner (Grossman et al., 2004).”
• Tumor‐induced tolerance and immune suppression by myeloid derived suppressor cells (2008, background): “IDO expression inhibits effector T cells and can activate Treg cells, inducing a suppressive microenvironment within the tumor; moreover, Treg cells express cytotoxic Tlymphocyte antigen-4 (CTLA4) on their surface, which can bind CD80 molecules expressed on DC subsets, and upregulate IDO protein exp”
• CTLA-4 and PD-1 Receptors Inhibit T-Cell Activation by Distinct Mechanisms (2004, background): “During this transition, T cells are vulnerable to inhibition by events that limit the supply of metabolites such as glucose and tryptophan (28).”
• Expression of indoleamine 2,3-dioxygenase by plasmacytoid dendritic cells in tumor-draining lymph nodes. (2004, background): “Previously, we have reported that pDCs constitute one of the " IDO-competent " subsets of DCs, able to upregulate IDO (by immunohistochemistry) in response to CTLA4-Ig treatment (58).”
• Indoleamine 2,3-dioxygenase is a critical resistance mechanism in antitumor T cell immunotherapy targeting CTLA-4 (2013, background): “In addition to being constitutively expressed by many malignant cells (Muller et al., 2005a), IDO can be induced in tumor cells and APCs by proinflammatory stimuli such as IFN-, which is generated by the host immune response against the tumor (Taylor and Feng, 1991; Belladonna et al., 2009).”