CD366 (TIM3) Monoclonal Antibody (F38-2E2), FITC, eBioscience™, Invitrogen™

Description

• Description: This F38-2E2 monoclonal antibody reacts with human CD366, also known as T cell immunoglobulin and mucin domain-containing protein 3 (TIM3) or HAVCR2
• This cell surface receptor is expressed on activated CD4+ T cell subsets (e.g
• Th1, Th17, and Treg), CD8+ T cells, monocytes, dendritic cells, and mast cells
• Due to alternative splicing, CD366 exists as membrane-bound and soluble forms
• Galectin-9 has been identified as the ligand for CD366
• In humans, this receptor negatively regulates CD4+ T cells, influencing the secretion of some Th1- and Th17-related cytokines
• CD366 has also been implicated in tolerance, autoimmune disease (e.g
• multiple sclerosis), and HIV infection
• Applications Reported: This F38-2E2 antibody has been reported for use in flow cytometric analysis
• Applications Tested: This F38-2E2 antibody has been pre-titrated and tested by flow cytometric analysis of stimulated normal human peripheral blood cells
• This can be used at 5 μL (0.125 μg) per test
• A test is defined as the amount (μg) of antibody that will stain a cell sample in a final volume of 100 μL
• Cell number should be determined empirically but can range from 10^5 to 10^8 cells/test
• Excitation: 488 nm; Emission: 520 nm; Laser: Blue Laser
• Filtration: 0.2 μm post-manufacturing filtered
• TIM3 (Hepatitis A virus cellular receptor 2, HAVCR2, T-cell immunoglobulin, mucin-dmain containing-3) is a 281 amino acid long, Type-1 Th1- specific cell surface glycoprotein expressed on terminally differentiated CD4+Th1 and CD8+Tc1 cells
• TIM3 consists of an IgV-like domain, a mucin-like domain in the extracellular region, and a conserved Tyrosine phosphorylation motif in the cytoplasmic region
• TIM3 is involved in macrophage activation and induction of autoimmune diseases
• Further, TIM3 down-regulates aggressive Th1-mediated immune responses and facilitates in the development of immune tolerance
• Pathological significance of TIM3 has been attributed to Experimental autoimmune encephalomyelitis (EAE), a Th-1 dependent autoimmune disease, and also enhances the severity of experimental autoimmune encephalomyelitis in mice.