Anti-Galectin-9 Rabbit pAb

Uncategorized

Ambient temperature

Stable for 12 months from date of receipt/reconstitution.

Galectin-9 is induced by proinflammatory stimuli, including IFN-γ, TNF-α, and TLR ligands, and regulates various immune responses through interaction with its ligand TIM-3. Binding of galectin-9 to TIM-3 expressed by Th1 CD4 T cells resulted in T cell death. On the other hand, galectin-9 treatment of tumor-bearing mice increased the number of IFN-γ-producing TIM-3+ CD8 T cells and TIM-3+ dendritic cells. Transgenic overexpression of either TIM-3 or galectin-9 in mice led to an increase in cells with a myeloid-derived suppressor cell phenotype and inhibition of immune responses. CD44 is also proposed to be a receptor for galectin-9, and interaction of galectin-9 with CD44 expressed by induced regulatory T (iTreg) cells enhanced the stability of function of iTreg cells. In addition, galectin-9 was recently demonstrated to bind Dectin-1 expressed by pancreatic ductal adenocarcinoma-infiltrating macrophages, resulting in tolerogenic macrophage reprogramming and suppression of anti-tumor immunity. Increased galectin-9 expression has been observed in several cancer types, including lung, liver, breast, and kidney.

PBS, Glycerol, BSA

Polyclonal

Cytoplasm, Nucleus, Secreted