Flow cytometric analysis of Jurkat cells (blue) and primary CD4+ T cells (green) using TIM-3 (D5D5R™) XP® Rabbit mAb (PE Conjugate). Controls were run on Jurkat cells (orange) and primary CD4+ T cells (red) using concentration-matched Rabbit (DA1E) mAb IgG XP® Isotype Control (PE Conjugate) #5742. CD4+ T cells were purified from human blood and stimulated for 9 days using beads coated with CD3 and CD28 antibodies in the presence of Human Interleukin-2 (hIL-2) #8907 (6.7 ng/ml).Learn more about how we get our images.
NOTE: Account for isotype matched controls for monoclonal antibodies or species matched IgG for polyclonal antibodies. Count cells using a hemacytometer or alternative method.
revised April 2016
Protocol Id: 1104
Supplied in PBS (pH 7.2), less than 0.1% sodium azide and 2 mg/ml BSA. Store at 4°C. Do not aliquot the antibody. Protect from light. Do not freeze.
TIM-3 (D5D5R™) XP® Rabbit mAb (PE Conjugate) recognizes endogenous levels of total TIM-3 protein.
Monoclonal antibody is produced by immunizing animals with recombinant protein specific to the extracellular domain of human TIM-3 protein.
This Cell Signaling Technology antibody is conjugated to phycoerythrin (PE) and tested in-house for direct flow cytometry analysis in human cells. This antibody is expected to exhibit the same species cross-reactivity as the unconjugated TIM-3 (D5D5R™) XP® Rabbit mAb #45208.
T cell Ig- and mucin-domain-containing molecules (TIMs) are a family of transmembrane proteins expressed by various immune cells. TIM-3 is an inhibitory molecule that is induced following T cell activation (1-3 ). TIM-3 is expressed by exhausted T cells in the settings of chronic infection and cancer (4,5), and tumor-infiltrating T cells that coexpress PD-1 and TIM-3 exhibit the most severe exhausted phenotype (5). Tumor-infiltrating dendritic cells (DCs) also express TIM-3. TIM-3 expression on DCs was found to suppress innate immunity by reducing the immunogenicity of nucleic acids released by dying tumor cells (6). Research studies show that heterodimerization of TIM-3 with CEACAM-1 is critical for the inhibitory function of TIM-3, and co-blockade of TIM-3 and CEACAM-1 enhanced antitumor responses in a mouse model of colorectal cancer (7). In addition, blockade of TIM-3 in mouse models of autoimmunity enhanced the severity of disease (1). Finally, binding of Galectin-9 to TIM-3 expressed by Th1 cells induces T cell death (8).
Cell Signaling Technology is a trademark of Cell Signaling Technology, Inc. XP is a registered trademark of Cell Signaling Technology, Inc.
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