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AB155379

APC Anti-TIM 3 antibody [F38-2E2]

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(2 Publications)

Mouse Monoclonal TIM 3 antibody - conjugated to APC. Suitable for Flow Cyt and reacts with Human samples. Cited in 2 publications. Immunogen corresponding to Recombinant Fragment Protein within Human HAVCR2.

View Alternative Names

CD366, TIM3, TIMD3, HAVCR2, Hepatitis A virus cellular receptor 2, HAVcr-2, T-cell immunoglobulin and mucin domain-containing protein 3, T-cell immunoglobulin mucin receptor 3, T-cell membrane protein 3, TIMD-3, TIM-3

1 Images
Flow Cytometry - APC Anti-TIM 3 antibody [F38-2E2] (AB155379)
  • Flow Cyt

Unknown

Flow Cytometry - APC Anti-TIM 3 antibody [F38-2E2] (AB155379)

Flow Cytometric analysis of unstimulated (left) or anti-Human CD3 and anti-Human CD28 stimulated (right) normal Human peripheral blood cells with anti-Human CD4 FITC and ab155379 at 0.06 μg. Total viable cells, as determined by Fixable Viability Dye eFluor® 780, were used for analysis.

Key facts

Host species

Mouse

Clonality

Monoclonal

Clone number

F38-2E2

Isotype

IgG1

Light chain type

kappa

Conjugation

APC

Excitation/Emission

Ex: 650nm, Em: 660nm

Carrier free

No

Reacts with

Human

Applications

Flow Cyt

applications

Immunogen

Recombinant Fragment Protein within Human HAVCR2. The exact immunogen used to generate this antibody is proprietary information.

Q8TDQ0

Reactivity data

{ "title": "Reactivity Data", "filters": { "stats": ["", "Species", "Dilution Info", "Notes"], "tabs": { "all-applications": {"fullname" : "All Applications", "shortname": "All Applications"}, "FlowCyt" : {"fullname" : "Flow Cytometry", "shortname":"Flow Cyt"} }, "product-promise": { "all": "all", "testedAndGuaranteed": "tested", "guaranteed": "expected", "predicted": "predicted", "notRecommended": "not-recommended" } }, "values": { "Human": { "FlowCyt-species-checked": "testedAndGuaranteed", "FlowCyt-species-dilution-info": "5 µL for 10^6 Cells", "FlowCyt-species-notes": "<p><a href='/en-us/products/primary-antibodies/apc-mouse-fab2-igg1-kappa-monoclonal-15h6-isotype-control-ab37391'>ab37391</a> - Mouse monoclonal IgG1, is suitable for use as an isotype control with this antibody.</p>" } } }

Properties and storage information

Form
Liquid
Purification technique
Affinity purification Protein G
Storage buffer
pH: 7.2 Preservative: 0.09% Sodium azide Constituents: PBS, 0.2% BSA
Shipped at conditions
Blue Ice
Appropriate short-term storage conditions
+4°C
Appropriate long-term storage conditions
+4°C

Supplementary information

This supplementary information is collated from multiple sources and compiled automatically.

TIM-3 also known as T cell immunoglobulin and mucin-domain containing-3 or HAVCR2 is a protein involved in immune regulation. It possesses an approximate mass of 35 kDa. TIM-3 is expressed on various immune cells including T cells NK cells and dendritic cells especially after activation. The expression level often changes in response to inflammatory conditions suggesting its role in modulating immune responses.
Biological function summary

TIM-3 functions as a checkpoint inhibitor impacting immune cell activity. It is not part of a larger physical complex but it modulates immune responses by interacting with its ligands such as Galectin-9 phosphatidylserine and CEACAM1. TIM-3 involvement in downregulating Th1 cell responses shows its necessary role in maintaining immune homeostasis. The protein also acts in regulating tolerance mechanisms and preventing autoimmunity.

Pathways

TIM-3 participation is seen in the immune checkpoint and T cell exhaustion pathways. TIM-3 signaling results in T cell inhibition affecting the PD-1 pathway as well. It shares a relationship with proteins like LAG-3 and PD-1 which are key to immune inhibitory signaling. These interactions depict TIM-3's role in immune tolerance during chronic infections and malignancies.

TIM-3 association with cancer and chronic infections provides insight into therapeutic implications. In cancer TIM-3 contributes to immune evasion often co-expressed with PD-1 leading to T cell exhaustion. In autoimmune diseases TIM-3 modulation may affect disease progression by influencing immune tolerance. Understanding TIM-3's role in these contexts aids in developing targeted therapies such as anti-TIM-3 antibodies to enhance immune responses in cancer while promoting tolerance in autoimmunity.

Product protocols

For this product, it's our understanding that no specific protocols are required. You can visit:

Target data

Cell surface receptor implicated in modulating innate and adaptive immune responses. Generally accepted to have an inhibiting function. Reports on stimulating functions suggest that the activity may be influenced by the cellular context and/or the respective ligand (PubMed : 24825777). Regulates macrophage activation (PubMed : 11823861). Inhibits T-helper type 1 lymphocyte (Th1)-mediated auto- and alloimmune responses and promotes immunological tolerance (PubMed : 14556005). In CD8+ cells attenuates TCR-induced signaling, specifically by blocking NF-kappaB and NFAT promoter activities resulting in the loss of IL-2 secretion. The function may implicate its association with LCK proposed to impair phosphorylation of TCR subunits, and/or LGALS9-dependent recruitment of PTPRC to the immunological synapse (PubMed : 24337741, PubMed : 26492563). In contrast, shown to activate TCR-induced signaling in T-cells probably implicating ZAP70, LCP2, LCK and FYN (By similarity). Expressed on Treg cells can inhibit Th17 cell responses (PubMed : 24838857). Receptor for LGALS9 (PubMed : 16286920, PubMed : 24337741). Binding to LGALS9 is believed to result in suppression of T-cell responses; the resulting apoptosis of antigen-specific cells may implicate HAVCR2 phosphorylation and disruption of its association with BAG6. Binding to LGALS9 is proposed to be involved in innate immune response to intracellular pathogens. Expressed on Th1 cells interacts with LGALS9 expressed on Mycobacterium tuberculosis-infected macrophages to stimulate antibactericidal activity including IL-1 beta secretion and to restrict intracellular bacterial growth (By similarity). However, the function as receptor for LGALS9 has been challenged (PubMed : 23555261). Also reported to enhance CD8+ T-cell responses to an acute infection such as by Listeria monocytogenes (By similarity). Receptor for phosphatidylserine (PtSer); PtSer-binding is calcium-dependent. May recognize PtSer on apoptotic cells leading to their phagocytosis. Mediates the engulfment of apoptotic cells by dendritic cells. Expressed on T-cells, promotes conjugation but not engulfment of apoptotic cells. Expressed on dendritic cells (DCs) positively regulates innate immune response and in synergy with Toll-like receptors promotes secretion of TNF-alpha. In tumor-imfiltrating DCs suppresses nucleic acid-mediated innate immune repsonse by interaction with HMGB1 and interfering with nucleic acid-sensing and trafficking of nucleid acids to endosomes (By similarity). Expressed on natural killer (NK) cells acts as a coreceptor to enhance IFN-gamma production in response to LGALS9 (PubMed : 22323453). In contrast, shown to suppress NK cell-mediated cytotoxicity (PubMed : 22383801). Negatively regulates NK cell function in LPS-induced endotoxic shock (By similarity).
See full target information HAVCR2

Publications (2)

Recent publications for all applications. Explore the full list and refine your search

iScience 27:108957 PubMed38333692

2024

EP300 restores the glycolytic activity and anti-tumor function of CD8 cytotoxic T cells in nasopharyngeal carcinoma.

Applications

Unspecified application

Species

Unspecified reactive species

Zhixiu Xia,Xiaoxu Ding,Chao Ji,Dabo Zhou,Xun Sun,Tiancong Liu

Tissue engineering and regenerative medicine 19:1321-1336 PubMed36074328

2022

The Combination of Platelet Rich Plasma Gel, Human Umbilical Mesenchymal Stem Cells and Nanohydroxyapatite/polyamide 66 Promotes Angiogenesis and Bone Regeneration in Large Bone Defect.

Applications

Unspecified application

Species

Unspecified reactive species

Wei Liu,Yong Huang,Daqian Liu,Teng Zeng,Jingzhe Wang,Ang Li,Dawei Wang,Xiaoyu Wang
View all publications

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