InVivoMAb anti-mouse Galectin-9
About InVivoMAb anti-mouse Galectin-9
The RG9-1 monoclonal antibody reacts with mouse galectin-9 a 40 kDa S-type lectin that is expressed by various cell types including lymphocytes, thymocytes, macrophages, dendritic cells, astrocytes, mast cells, eosinophils, fibroblasts, epithelial cells, and endothelial cells. Galectin-9 binds to β-galactosides and can serve as a ligand for TIM-3 (CD366). The protein is implicated in both innate and adaptive immune responses specifically, induction of cytokine secretion by macrophages, bactericidal functions, promotion of dendritic cell maturation, regulatory T cell expansion, and negative regulation of Th1, Th17, NK, and cytotoxic T cells. The RG9-35 antibody has been reported to block some biological activities of Galectin-9 when administered in vivo.
InVivoMAb anti-mouse Galectin-9 Specifications
Rat IgG2b, κ
|Recommended Isotype Control(s)||InVivoMAb rat IgG2b isotype control, anti-keyhole limpet hemocyanin(BE0090)|
|Recommended InVivoPure Dilution Buffer||InVivoPure pH 7.0 Dilution Buffer(IP0070)|
Recombinant mouse galectin-9
in vivo Galectin-9 blockade
0.2 μM filtered
Purified from tissue culture supernatant in an animal free facility
The antibody solution should be stored undiluted at 4°C, and protected from prolonged exposure to light. Do not freeze.
InVivoMAb anti-mouse Galectin-9 (Clone: RG9-1)Dolina, J. S., et al. (2014). "Liver-primed CD8+ T cells suppress antiviral adaptive immunity through galectin-9-independent T-cell immunoglobulin and mucin 3 engagement of high-mobility group box 1 in mice." Hepatology 59(4): 1351-1365. PubMed
The liver is a tolerogenic environment exploited by persistent infections, such as hepatitis B (HBV) and C (HCV) viruses. In a murine model of intravenous hepatotropic adenovirus infection, liver-primed antiviral CD8(+) T cells fail to produce proinflammatory cytokines and do not display cytolytic activity characteristic of effector CD8(+) T cells generated by infection at an extrahepatic, that is, subcutaneous, site. Importantly, liver-generated CD8(+) T cells also appear to have a T-regulatory (Treg) cell function exemplified by their ability to limit proliferation of antigen-specific T-effector (Teff ) cells in vitro and in vivo via T-cell immunoglobulin and mucin 3 (Tim-3) expressed by the CD8(+) Treg cells. Regulatory activity did not require recognition of the canonical Tim-3 ligand, galectin-9, but was dependent on CD8(+) Treg cell-surface Tim-3 binding to the alarmin, high-mobility group box 1 (HMGB-1). CONCLUSION: Virus-specific Tim-3(+) CD8(+) T cells operating through HMGB-1 recognition in the setting of acute and chronic viral infections of the liver may act to dampen hepatic T-cell responses in the liver microenvironment and, as a consequence, limit immune-mediated tissue injury or promote the establishment of persistent infections.