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Lymphocyte-activation gene 3

LAG-3, CD223
Lymphocyte-activation protein 3 belongs to Ig superfamily and contains 4 extracellular Ig-like domains. The LAG3 gene contains 8 exons. The sequence data, exon/intron organization, and chromosomal localization all indicate a close relationship of LAG3 to CD4. [provided by RefSeq, Jul 2008] (from NCBI)
Top mentioned proteins: CD4, CD8, CTLA-4, MHC, CAN
Papers on LAG-3
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).
Expression of PD-1/LAG-3 and cytokine production by CD4(+) T cells during infection with Plasmodium parasites.
Yui et al., Nagasaki, Japan. In Microbiol Immunol, Jan 2016
CD4(+) T cells from mice infected with P. yoelii 17XL, P yoelii 17XNL, P. chabaudi, P. vinckei, and P. berghei expressed the inhibitory receptors, PD-1 and LAG-3 as early as 6 days after infection, while those from either Listeria monocytogenes or Leishmania major-infected mice did not.
Activated T cells sustain myeloid-derived suppressor cell-mediated immune suppression.
Mandruzzato et al., Padova, Italy. In Oncotarget, Jan 2016
Finally, we show that the expression of ligands B7-H1 and MHC class II both on in vitro-induced MDSCs and on MDSCs in the tumor microenvironment of cancer patients is paralleled by an increased expression of their respective receptors PD-1 and LAG-3 on T cells, two inhibitory molecules associated with T cell dysfunction.
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.
Aire-Overexpressing Dendritic Cells Induce Peripheral CD4⁺ T Cell Tolerance.
Yang et al., Changchun, China. In Int J Mol Sci, Dec 2015
We demonstrated that Aire cells upregulated the mRNA levels of the tolerance-related molecules CD73, Lag3, and FR4 and the apoptosis of CD4⁺ T cells in STZ-T1D mouse-derived splenocytes.
Emerging targets in cancer immunotherapy: beyond CTLA-4 and PD-1.
Zang et al., New York City, United States. In Immunotherapy, Nov 2015
PD-L1 inhibitors and LAG-3 inhibitors have progressed through clinical trials.
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.
Clinical blockade of PD1 and LAG3--potential mechanisms of action.
Ohashi et al., Toronto, Canada. In Nat Rev Immunol, 2015
In this Review, we discuss the potential mechanisms of action of the clinical agents that target two of these receptors, programmed cell death protein 1 (PD1) and lymphocyte activation gene 3 protein (LAG3).
An Immunocompetent Mouse Model for MLL/AF9 Leukemia Reveals the Potential of Spontaneous Cytotoxic T-Cell Response to an Antigen Expressed in Leukemia Cells.
Hosen et al., Suita, Japan. In Plos One, 2014
In mice with advanced leukemia, antigen-specific CTLs were also expanded, but were unresponsive to antigen stimulation and expressed high levels of PD-1 and LAG-3.
WNT5A transforms intestinal CD8αα(+) IELs into an unconventional phenotype with pro-inflammatory features.
Ran et al., Shanghai, China. In Bmc Gastroenterol, 2014
The non-canonical WNT5A skewed them into a pro-inflammatory category as measured by inhibitory cell surface marker LAG3, LY49E, NKG2A and activated marker CD69 and FASL.
[Immunotherapy for the Prevention and Treatment of Breast Cancer].
Slabý et al., In Klin Onkol, 2014
CTLA-4, PD-1/ PD-L1, LAG3).
Coexpression of CD49b and LAG-3 identifies human and mouse T regulatory type 1 cells.
Roncarolo et al., Milano, Italy. In Nat Med, 2013
By gene expression profiling of human Tr1 cell clones, we identified the surface markers CD49b and lymphocyte activation gene 3 (LAG-3) as being stably and selectively coexpressed on mouse and human Tr1 cells.
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
Bat3-deficient T cells have elevated expression of exhaustion-associated molecules such as Tim-3, Lag3, Prdm1 and Pbx3, and Bat3 knockdown in myelin-antigen–specific CD4+ T cells markedly inhibits the development of experimental autoimmune encephalomyelitis while promoting the expansion of a dysfunctional Tim-3hi, interferon-γ (IFN-γ)loCD4+ cell population.
Immune inhibitory molecules LAG-3 and PD-1 synergistically regulate T-cell function to promote tumoral immune escape.
Vignali et al., Memphis, United States. In Cancer Res, 2012
these results define a strong synergy between the PD-1 and LAG-3 inhibitory pathways in tolerance to both self and tumor antigens.
Therapeutic blockade of PD-L1 and LAG-3 rapidly clears established blood-stage Plasmodium infection.
Harty et al., Iowa City, United States. In Nat Immunol, 2012
In vivo blockade of the PD-1 ligand PD-L1 and the inhibitory receptor LAG-3 restored CD4(+) T cell function, amplified the number of follicular helper T cells and germinal-center B cells and plasmablasts, enhanced protective antibodies and rapidly cleared blood-stage malaria in mice.
Cutting edge: accelerated autoimmune diabetes in the absence of LAG-3.
Vignali et al., Memphis, United States. In J Immunol, 2011
We conclude that LAG-3 is necessary for regulating CD4(+) and CD8(+) T cell function during autoimmune diabetes
LAG-3, TGF-β, and cell-intrinsic PD-1 inhibitory pathways contribute to CD8 but not CD4 T-cell tolerance induced by allogeneic BMT with anti-CD40L.
Sykes et al., Boston, United States. In Blood, 2011
LAG-3 is required for long-term peripheral CD8 but not CD4 T-cell tolerance and this requirement is CD8 cell-extrinsic.
MHC class II engagement by its ligand LAG-3 (CD223) contributes to melanoma resistance to apoptosis.
Michel et al., Paris, France. In J Immunol, 2011
our data suggest that the LAG-3-MHC II interaction could be viewed as a bidirectional immune escape pathway in melanoma
PD-1 and LAG-3 inhibitory co-receptors act synergistically to prevent autoimmunity in mice.
Honjo et al., Tokushima, Japan. In J Exp Med, 2011
LAG-3 acts synergistically with PD-1 and/or other immunoregulatory genes to prevent autoimmunity in mice.
Coregulation of CD8+ T cell exhaustion by multiple inhibitory receptors during chronic viral infection.
Wherry et al., Philadelphia, United States. In Nat Immunol, 2009
Regulation of T cell exhaustion by various inhibitory pathways was nonredundant, as blockade of the T cell inhibitory receptors PD-1 and LAG-3 simultaneously and synergistically improved T cell responses and diminished viral load in vivo.
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