Interaction of Tim-3 and Tim-3 ligand regulates T helper type 1 responses and induction of peripheral tolerance
By C. A. Sabatos, S. Chakravarti, Eugene K. Cha, A. Schubart, A. Sánchez‐Fueyo, X. Zheng, A. Coyle, T. Strom, G. Freeman, V. Kuchroo. Nature Immunology, 2003
677 citations recorded by the source corpus.
Subfields: Immunology, Molecular Biology
View Paper: https://www.semanticscholar.org/paper/7f0a219673041fb7f9bd67a22cce92d930d1e387
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In Immunology
In Molecular Biology
Citations in the corpus
- OMIP‐037: 16‐color panel to measure inhibitory receptor signatures from multiple human immune cell subsets (2017, background): “Also, NK cytotoxicity is abrogated upon TIM-3 cross-linking in vitro (18), and TIM-3 signaling is integral for tolerance induction and EAE amelioration in mouse models (17,19,20).”
- The Tim-3 ligand galectin-9 negatively regulates T helper type 1 immunity (2005, background): “First, blocking this pathway with a Tim-3–Ig fusion protein during an ongoing immune response results in hyperproliferation of T H 1 cells, with massive spontaneous production of IFN-&gamma”
- Upregulation of Tim-3 and PD-1 expression is associated with tumor antigen–specific CD8+ T cell dysfunction in melanoma patients (2010, background): “In mice, blocking the Tim-3–Tim-3L pathway resulted in hyperproliferation of Th1-type cells and abrogated the induction of peripheral and transplantation tolerance (Sabatos et al., 2003; Sánchez-Fueyo et al., 2003).”
- TIM genes: a family of cell surface phosphatidylserine receptors that regulate innate and adaptive immunity (2010, background): “Treatment with TIM-3 mAb strongly enhanced T-cell proliferation and IFN-c production and decreased IL-10 production in response to HCV peptide antigen (83).”