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TIM-3/HAVCR2   Protein, Antibody, ELISA Kit, cDNA Clone

発現宿主: Human Cells  
10390-H03H-50
10390-H03H-100
50 µg 
100 µg 
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発現宿主: Human Cells  
10390-H08H-50
10390-H08H-100
50 µg 
100 µg 
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発現宿主: Human Cells  
51152-M08H-50
51152-M08H-100
50 µg 
100 µg 
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発現宿主: Human Cells  
51152-M02H-50
51152-M02H-100
50 µg 
100 µg 
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発現宿主: Human Cells  
90312-C02H-50
90312-C02H-100
50 µg 
100 µg 
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  • Slide 1

TIM-3/HAVCR2  Related Area

TIM-3/HAVCR2  関連経路

    TIM-3/HAVCR2  サマリー & タンパク質情報

    TIM-3/HAVCR2  背景

    遺伝子の概要: The protein encoded by HAVCR2 gene belongs to the immunoglobulin superfamily, and TIM family of proteins. CD4-positive T helper lymphocytes can be divided into types 1 (Th1) and 2 (Th2) on the basis of their cytokine secretion patterns. Th1 cells are involved in cell-mediated immunity to intracellular pathogens and delayed-type hypersensitivity reactions, whereas, Th2 cells are involved in the control of extracellular helminthic infections and the promotion of atopic and allergic diseases. This protein is a Th1-specific cell surface protein that regulates macrophage activation, and inhibits Th1-mediated auto- and alloimmune responses, and promotes immunological tolerance. [provided by RefSeq, Sep 2011]
    General information above from NCBI
    細胞内位置: Membrane {ECO:0000305}; Single-pass type I membrane protein {ECO:0000305}.
    組織特異性: T-helper type 1 lymphocyte (Th1)-specific.
    翻訳後: O-glycosylated with core 1 or possibly core 8 glycans. {ECO:0000269|PubMed:22171320}.
    シーケンスの類似性: Belongs to the immunoglobulin superfamily. TIM family. {ECO:0000305}.; Contains 1 Ig-like V-type (immunoglobulin-like) domain. {ECO:0000305}.
    General information above from UniProt

    Hepatitis A virus cellular receptor 2 (HAVCR2), formerly known as T cell immunoglobulin and mucin domain-3 (TIM-3), is a transmembrane glycoprotein expressed on the surface of terminally differentiated Th1 cells but not on Th2 cells. It was the first surface molecule that specifically identifies Th1 cells in both mice and human. Recently, identification of Galectin-9 as a ligand for TIM-3 has established the TIM-3-Galectin-9 pathway as an important regulator of Th1 immunity and tolerance induction. Engagement of Tim-3 by its ligand galectin-9 negatively regulates IFN-gamma secretion and influences the ability to induce T cell tolerance in both mice and man. It suggests a novel paradigm in which dysregulation of the TIM-3-galectin-9 pathway could underlie chronic autoimmune disease states, such as multiple sclerosis. Recent work has explored the role of TIM-3 in systemic lupus erythematosus (SLE), and their results indicate that TIM-3 may represent a novel target for the treatment of SLE. Numerous studies have demonstrated that Tim-3 influences autoimmune diseases, including diabetes and multiple sclerosis, and its role in other inflammatory diseases including allergies and cancer is beginning to become clear. In tumor rejection model, soluble form of Tim-3 (sTim-3) significantly impaired T cell antitumor immunity, evidenced by decreased antitumor CTL activity and reduced amount of tumor-infiltrating lymphocytes in tumor. sTim-3 as an immunoregulatory molecule that may be involved in the negative regulation of T cell-mediated immune response.

    Immune Checkpoint
    Immune Checkpoint Detection: ELISA Antibodies   Immune Checkpoint Detection: IP Antibodies   Immune Checkpoint Detection: WB Antibodies
    Immune Checkpoint Proteins
    Immune Checkpoint Targets   Co-inhibitory Immune Checkpoint Targets

    Immunotherapy   Cancer Immunotherapy   Targeted Therapy

    TIM-3/HAVCR2  代替名

    TIM-3/HAVCR2  関連研究

  • Geng H, et al. (2006) Soluble form of T cell Ig mucin 3 is an inhibitory molecule in T cell-mediated immune response. J Immunol. 176(3): 1411-20.
  • Anderson AC, et al. (2006) TIM-3 in autoimmunity. Curr Opin Immunol. 18(6): 665-9.
  • Anderson DE. (2007) TIM-3 as a therapeutic target in human inflammatory diseases. Expert Opin Ther Targets. 11(8): 1005-9.
  • Pan HF, et al. (2010) TIM-3 as a new therapeutic target in systemic lupus erythematosus. Mol Biol Rep. 37(1): 395-8.
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