Editorial: Tim-3 puts on the brakes Ana Carrizosa Anderson 1 Brigham and Women's Hospital and Harvard Medical School, Boston, Massachusetts, USA ↵ 1. Correspondence: Brigham and Women's Hospital and Harvard Medical School, Boston, MA 02115, USA. E-mail: aanderson@rics.bwh.harvard.edu regulatory cell surface molecules immune response IFN-γ-producing CD4 + Th1 cells are critically important for immunity against intracellular pathogens and in fighting cancer; however, an uncontrolled Th1 immune response can result in undesirable immunopathology. Tim-3 was discovered nearly 10 years ago as a molecule expressed on Th1 and Tc1 cells but not on other Th and Tc subsets [ 1 ]. Upon interaction with its ligand, galectin-9, Tim-3 induces a death signal in Th1 cells [ 2 ], thereby contracting Th1 immune responses and preventing the immunopathology that would otherwise ensue. Tim-3 can therefore be classed along with other negative regulatory receptors such as CTLA-4 and PD-1, which are also expressed on T cells and serve to contract T cell responses. The notable difference between Tim-3 and these other negative regulatory receptors is that Tim-3 expression is restricted to Th1 and Tc1 cells, whereas the others are expressed on all T cells. Collectively, these negative regulatory receptors are now commonly
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