gopubmed logo
find other proteinsAll proteins
GoPubMed Proteins lists recent and important papers and reviews for proteins. Page last changed on 19 Dec 2016.

Hepatitis A virus cellular receptor 2

The protein encoded by this 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] (from NCBI)
Top mentioned proteins: galectin-1, CD8, galectin-9, CD4, CAN
Papers on Tim-3
Characterization of age-associated exhausted CD8(+) T cells defined by increased expression of Tim-3 and PD-1.
Kang et al., Seoul, South Korea. In Aging Cell, Feb 2016
In this study, we demonstrate that T-cell immunoglobulin mucin domain-3 (Tim-3), another exhaustion marker, is up-regulated on aged T cells, especially CD8(+) T cells.
Role of Regulatory T Cells and Inhibitory Molecules in the Development of Immune Exhaustion During Human Immunodeficiency Virus Type 1 Infection.
Rugeles et al., Medellín, Colombia. In Viral Immunol, Jan 2016
One of the key hallmarks of chronic human immunodeficiency virus type 1 (HIV-1) infection is the persistent immune activation triggered since early stages of the infection, followed by the development of an exhaustion phenomena, which leads to the inability of immune cells to respond appropriately to the virus and other pathogens, constituting the acquired immunodeficiency syndrome (AIDS); this exhausting state is characterized by a loss of effector functions of immune cells such as proliferation, production of cytokine, as well as cytotoxic potential and it has been attributable to an increased response of regulatory T cells and recently also to the expression in different cell populations of inhibitory molecules, such as programmed death receptor-1 (PD-1), cytotoxic T lymphocyte antigen-4 (CTLA-4), T cell immunoglobulin-3 (Tim-3), and lymphocyte activation gene-3 (LAG-3).
Systemic immune activity predicts overall survival in treatment naïve patients with metastatic pancreatic cancer.
Lesinski et al., Hem, France. In Clin Cancer Res, Jan 2016
HR=1.53), the TIM3 molecule had a positive association with survival when expressed on CD4+ T cells (p=0.046;
Interleukin 10-expressing B cells inhibit tumor-infiltrating T cell function and correlate with T cell Tim-3 expression in renal cell carcinoma.
Sun et al., Shanghai, China. In Tumour Biol, Jan 2016
The expression of T cell exhaustion marker Tim-3, however, was upregulated in patients with high frequencies of IL-10-producing B cells.
Targeting immune checkpoints: New opportunity for mesothelioma treatment?
Smits et al., Antwerp, Belgium. In Cancer Treat Rev, Dec 2015
Here, we discuss the expression patterns and mechanisms of action of CTLA-4 and PD-1 as the two most studied and of TIM-3 and LAG-3 as two interesting upcoming immune checkpoints.
Tim-3 Is Upregulated in NK Cells during Early Pregnancy and Inhibits NK Cytotoxicity toward Trophoblast in Galectin-9 Dependent Pathway.
Qu et al., Jinan, China. In Plos One, Dec 2015
T cell Ig and mucin domain-containing protein 3 (Tim-3) is a newly defined molecule with essential immunological function in many physiological and pathological processes.
Identification of TIM-3 as a Leukemic Stem Cell Surface Molecule in Primary Acute Myeloid Leukemia.
Miyamoto et al., Fukuoka, Japan. In Oncology, Nov 2015
T-cell immunoglobulin mucin-3 (TIM-3) is expressed in most types of AML LSCs, but not in normal hematopoietic stem cells (HSCs); therefore, TIM-3 would be one of the promising therapeutic targets to specifically kill AML LSCs, sparing normal HSCs.
Emerging immune checkpoints for cancer therapy.
Wu et al., Changzhou, China. In Acta Oncol, Nov 2015
LAG-3 and TIM-3 are two new immune checkpoints.
[Progress of molecular genetics research on rheumatoid arthritis].
Zhang et al., Nanchong, China. In Zhonghua Yi Xue Yi Chuan Xue Za Zhi, Oct 2015
In addition to genes from human leukocyte antigen (HLA) region, such as HLA-DRB, genes from non-HLA region, such as TIM-3, PTPN22, TRAF1/C5, STAT4, CCR5, PADI4 and FCGR2A may also contribute to its susceptibility.
A TIM-3/Gal-9 Autocrine Stimulatory Loop Drives Self-Renewal of Human Myeloid Leukemia Stem Cells and Leukemic Progression.
Akashi et al., Fukuoka, Japan. In Cell Stem Cell, Oct 2015
T-cell immunoglobin mucin-3 (TIM-3) is expressed on the surface of LSCs in many types of human acute myeloid leukemia (AML), but not on hematopoietic stem cells (HSCs).
CEACAM1 regulates TIM-3-mediated tolerance and exhaustion.
Blumberg et al., Boston, United States. In Nature, Feb 2015
T-cell immunoglobulin domain and mucin domain-3 (TIM-3, also known as HAVCR2) is an activation-induced inhibitory molecule involved in tolerance and shown to induce T-cell exhaustion in chronic viral infection and cancers.
Roles of PD-1, Tim-3 and CTLA-4 in immunoregulation in regulatory T cells among patients with sepsis.
Qi et al., Dalian, China. In Int J Clin Exp Med, 2014
OBJECTIVE: This study aims to elucidate the roles of PD-1, Tim-3 and CTLA-4 in sepsis.
Bat3 promotes T cell responses and autoimmunity by repressing Tim-3–mediated cell death and exhaustion.
Kuchroo et al., Boston, United States. In Nat Med, 2012
T cell immunoglobulin and mucin domain–containing 3 (Tim-3) is an inhibitory receptor that is expressed on exhausted T cells during infection with HIV-1 and hepatitis C virus.
Tumor-infiltrating DCs suppress nucleic acid-mediated innate immune responses through interactions between the receptor TIM-3 and the alarmin HMGB1.
Jinushi et al., Sapporo, Japan. In Nat Immunol, 2012
TIM-3 circumvents the stimulatory effects of nucleic acids in tumor immunity by interactding with HMGB1 to interfere with the recruitment of nucleic acids into dendritic cell endosomes
Contrasting acute graft-versus-host disease effects of Tim-3/galectin-9 pathway blockade dependent upon the presence of donor regulatory T cells.
Blazar et al., Minneapolis, United States. In Blood, 2012
These studies are the first to show that the absence of Tim-3/gal-9 pathway interactions augments systemic graft versus host disease and regulatory T-cells contributute to it.
T-cell immunoglobulin- and mucin-domain-containing molecule 3 gene polymorphisms and renal cell carcinoma.
Sun et al., Shanghai, China. In Dna Cell Biol, 2012
polymorphisms in the TIM-3 gene are new risk factors for RCC
Allograft rejection is restrained by short-lived TIM-3+PD-1+Foxp3+ Tregs.
Strom et al., Boston, United States. In J Clin Invest, 2012
the number and frequencey of FoxP3, TIM-3, PD-1 expressing Treg cells, present during allograft response, peaks at the time of graft rejection.
Blockade of Tim-3 signaling restores the virus-specific CD8⁺ T-cell response in patients with chronic hepatitis B.
Chen et al., Hangzhou, China. In Eur J Immunol, 2012
It was shown that Tim-3 negatively regulates antiviral responses of CD8+ T cells isolated from chronic hepatitis B patients, and this response is reversed by blocking the Tim-3 pathway.
Protective HIV-specific CD8+ T cells evade Treg cell suppression.
Horton et al., Seattle, United States. In Nat Med, 2011
This differential sensitivity of HIV-specific CD8(+) T cells to T(reg) cell-mediated suppression correlates with their expression of the inhibitory receptor T cell immunoglobulin domain and mucin domain 3 (Tim-3) after stimulation with their cognate epitopes.
share on facebooktweetadd +1mail to friends