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Transpl Immunol. 2008 Apr;19(1):12-9. doi: 10.1016/j.trim.2008.01.008. Epub 2008 Feb 20.

Activation of Tim-3-Galectin-9 pathway improves survival of fully allogeneic skin grafts.

Author information

1
Institute of Organ Transplantation, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei, China.

Abstract

T cell immunoglobulin and mucin domain (Tim)-3 is a molecule expressed on terminally differentiated murine Th1 cells but not on Th2 cells. Identification of Galectin-9 as a ligand for Tim-3 has now firmly established the Tim-3-Galectin-9 pathway as an important regulator of Th1 immunity, which results in apoptosis of Th1 cells. Here, we demonstrate that engagement of Tim-3 by mouse recombinant Galectin-9 remarkably suppresses allograft rejection and improves survival of allogeneic skin grafts. Furthermore, administration of recombinant Galectin-9 decreases Tim-3 positive cells in draining lymph node and selectively inhibits production of IFN-gamma after skin transplantation. At last, even low dose of Galectin-9 (1 microg/ml) can obviously inhibit TCR crosslinking-induced primary T cell proliferation in vitro. These observations suggest that Tim-3-Galectin-9 pathway plays an important role in the termination of productive Th1-immune response and could lead to developing novel therapies in transplant medicine.

PMID:
18346632
DOI:
10.1016/j.trim.2008.01.008
[Indexed for MEDLINE]

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