Human Tim-3 (CD366) Protein (C-His-Avi)

Human Tim-3 (C-His-Avi) Protein on SDS-PAGE under non-reducing (P-) and reducing (P+) conditions. The gel was stained for 1 hour with BlinkBlue Protein Staining Buffer (Catalog 700102). The purity of this protein appears to be greater than 95%.

Cat #	Size	Price	Quantity
602201	25 ug	$145
602202	100 ug	$295

Bulk/Custom

Product Details

Application	ELISA, BLI
Format	Liquid, Purified
Expression Host	CHO
Target Name	TIM3, HAVCR2, TIMD3, FLJ14428, KIM3
Species	Human
Accession Number	Q8TDQ0
Sources	Recombinant human Tim-3 protein (Ser22-Arg200) with C-terminus His-Avi tag was expressed in CHO Cells.
Molecular Weight	This protein has a predicted molecular weight of 23.7 kDa. Under DTT-reducing conditions, the protein migrates at approximately 45 kDa on SDS-PAGE.
Affinity Tag	C-His-Avi
Purity	>95% based on SDS-PAGE under reducing condition
Regulatory Status	RUO
Formulation	1xPBS buffer, pH7.4, 0.22 µm filtered
Endotoxin level	Not tested
Protein Concentration	25µg size is bottled at 0.2mg/mL concentration. 100 µg size is supplied at a lot-specific concentration.
Storage and Handling	Briefly centrifuge the vial upon receipt. An unopened vial can be stored at 4°C for up to 2 weeks, or at -20°C or below for up to six months. The protein may be further diluted to 0.1 mg/mL using 0.22 µm-filtered PBS buffer (pH 7.4). For long-term storage, the diluted stock solution should be aliquoted and stored at ≤ –70°C to minimize freeze-thaw cycles. If additional dilution is required, carrier proteins such as FBS or BSA should be added to maintain protein stability.
Research Areas	Immune Checkpoints, Th1 cells, Tregs, NK cells, conventional Dendritic cells, Macrophages, Monocytes, T cell Exhaustion, Autoimmunity, Cancer Immunology

Background Information

T cell immunoglobulin and mucin domain–containing protein 3 (Tim-3), also known as HAVCR2, is an inhibitory immune checkpoint receptor expressed on activated T cells, regulatory T cells (Tregs), natural killer (NK) cells, dendritic cells, and monocytes. Tim-3 plays a central role in regulating immune tolerance and limiting excessive inflammation. In chronic infection and cancer, sustained Tim-3 expression is a hallmark of T cell exhaustion, where effector T cells progressively lose proliferative capacity and cytokine production. Through inhibitory signaling pathways, Tim-3 dampens T cell receptor (TCR) signaling and modulates innate immune responses.

Structurally, Tim-3 is a type I transmembrane glycoprotein composed of an N-terminal immunoglobulin variable (IgV) domain, a mucin-like stalk region rich in O-linked glycosylation sites, a single transmembrane domain, and a cytoplasmic tail. Unlike PD-1, Tim-3 lacks classical ITIM or ITSM motifs; instead, its cytoplasmic tail contains conserved tyrosine residues that mediate signaling through adaptor proteins. In the absence of ligand engagement, the adaptor Bat3 associates with the cytoplasmic tail and maintains T cell activity. Ligand binding promotes Bat3 dissociation and recruitment of inhibitory signaling complexes, resulting in attenuated immune responses.

Tim-3 interacts with multiple ligands, reflecting its context-dependent functions. Key ligands include galectin-9, which can induce apoptosis of Th1 cells; phosphatidylserine, facilitating clearance of apoptotic cells; CEACAM1, which cooperatively regulates T cell inhibition; and HMGB1, modulating innate immune activation. These diverse interactions allow Tim-3 to regulate both adaptive and innate immunity.

Dysregulation of Tim-3 is implicated in cancer, chronic viral infections (such as HIV and hepatitis), autoimmune disorders, and inflammatory diseases. In tumors, Tim-3 is frequently co-expressed with PD-1 on exhausted T cells, contributing to immune escape. Elevated Tim-3 expression can also be observed in certain leukemias, where it may mark leukemic stem cells. Conversely, insufficient inhibitory signaling may exacerbate autoimmunity.

Therapeutically, Tim-3 is an emerging target in immuno-oncology. Monoclonal antibodies that block Tim-3 are being evaluated in clinical trials, often in combination with PD-1/PD-L1 inhibitors to overcome resistance to checkpoint blockade. Beyond oncology, modulating Tim-3 signaling may offer strategies to rebalance immune responses in chronic infection or autoimmune disease. As understanding of its signaling network deepens, Tim-3 remains a promising target for next-generation immune therapies.

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