TIM-3/HAVCR2 Protein, Mouse (Biotinylated, HEK293, His-Avi)

TIM-3/HAVCR2 protein, a cell surface receptor, plays a pivotal role in modulating both innate and adaptive immune responses. Predominantly considered as having an inhibitory function, the reported stimulating functions suggest a nuanced influence based on cellular context and ligand specificity. It regulates macrophage activation and inhibits T-helper type 1 lymphocyte (Th1)-mediated auto- and alloimmune responses, promoting immunological tolerance. In CD8+ cells, TIM-3 attenuates TCR-induced signaling by blocking NF-kappaB and NFAT promoter activities, leading to reduced IL-2 secretion. This inhibitory function is proposed to involve its association with LCK, impairing the phosphorylation of TCR subunits. Conversely, TIM-3 has been shown to activate TCR-induced signaling in T-cells, likely implicating ZAP70, LCP2, LCK, and FYN. The receptor for LGALS9, TIM-3's binding to LGALS9 is believed to suppress T-cell responses, leading to apoptosis of antigen-specific cells. Additionally, TIM-3 may recognize phosphatidylserine on apoptotic cells, mediating their phagocytosis, and positively regulates innate immune responses, particularly in dendritic cells. It also plays a role in suppressing nucleic acid-mediated innate immune responses in tumor-infiltrating dendritic cells and negatively regulates NK cell function in LPS-induced endotoxic shock. Interactions with various signaling molecules, including HMGB1, BAG6, PIK3R1, PIK3R2, FYN, and ILF3, further contribute to the intricate regulatory functions of TIM-3 in immune responses.