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Natural killer (NK) cells are lymphocytes that can mediate lysis of certain tumor cells and virus-infected cells without previous activation. Additionally we are shipping KLRG1 Antibodies (145) and KLRG1 Proteins (10) and many more products for this protein.
Treg cell accumulation in intestinal tumours from APC (show APC ELISA Kits)(min/+) mice was exclusively due to the increase in KLRG1(+) GATA3 (show GATA3 ELISA Kits)(+) Treg cells.
Although absence of KLRG1 is not enough to increase intestinal Treg cells in KLRG1 knockout mice, KLRG1 ligation reduces T-cell receptor signals and the competitive fitness of individual Treg cells in the intestine.
Ly6C, 4-1BB (show TNFRSF9 ELISA Kits), and KLRG1 have roles in the activation of lamina propria lymphocytes in the small intestine in a mouse model of Crohn's disease
This finding provides a rationale for the reciprocal expression of KLRG1 and CD103 (show ITGAE ELISA Kits) in different CD8 (show CD8A ELISA Kits)(+) T-cell subsets.
Cytotoxic KLRG1-expressed CD8 (show CD8A ELISA Kits) effector cells and defective T regulatory cells cause murine autoimmune cholangitis.
KLRG1(+) iNKT cells coexpressing CD49d and granzyme A (show GZMA ELISA Kits) persisted for several months and displayed a potent secondary response to cognate antigen.
high levels of TfRs such as those found on activated lymphocytes were found to be associated with decreased KLRG1 inhibitory function, indicating that TfRs may sequester KLRG1 from interacting with cadherins.
data further demonstrate that the inhibitory activity of KLRG1 is decreased in T cells expressing high levels of TfR (show TFRC ELISA Kits), indicating that association of KLRG1 with TfR (show TFRC ELISA Kits) hinders KLRG1-mediated silencing.
Data indicate that CD103 (show ITGAE ELISA Kits)(+)CD8 (show CD8A ELISA Kits)(+) T(RM) cells developed in the skin from epithelium-infiltrating precursor cells that lacked expression of the effector-cell marker KLRG1.
Data indicate that increments of CD8 (show CD8A ELISA Kits) + effector memory T cells in human and mouse chronic lymphocytic leukemia (CLL)(Emu-TCL1 (show TCL1A ELISA Kits) model) were due to an expansion of the inhibitory killer cell lectin-like receptor G1 (KLRG1) expressing cellular subset.
Killer Cell Lectin-like Receptor G1 Inhibits NK Cell Function through Activation of Adenosine 5'-Monophosphate-Activated Protein Kinase
The results suggest that a disease-associated SNP located within the 3'UTR (show UTS2R ELISA Kits) of KLRG1 directly interferes with miR (show MLXIP ELISA Kits)-584-5p binding, allowing for KLRG1 mRNA differential accumulation, which in turn may contribute to pathogenesis of pemphigus.
Demonstrate the presence of increased KLRG1-expressing T-cells in tuberculosis-treated individuals, and present KLRG1 as a marker of decreased human T-cell proliferation following BCG (show SLC11A1 ELISA Kits)-vaccination.
More T cells were KLRG1+ in the synovial fluid of patients with spondylarthritis/rheumatoid arthritis than crystal arthritis or controls. Those T cells were more functionally active, and migrated towards the synovial fluid of SpA (show FASL ELISA Kits)/RA patients.
KLRG1 was overexpressed on CD4 (show CD4 ELISA Kits)(+) T cells.
These results indicate that KLRG1 negatively regulates natural killer cell numbers and functions via the Akt (show AKT1 ELISA Kits) pathway, thus providing a novel marker and therapeutic target for hepatitis C virus infection.
cytomegalovirus positive had lower proportions of NK-cells expressing inhibitory receptors (KLRG1 and CD158a (show KIR2DL1 ELISA Kits))
Natural killer (NK) cells are lymphocytes that can mediate lysis of certain tumor cells and virus-infected cells without previous activation. They can also regulate specific humoral and cell-mediated immunity. The protein encoded by this gene belongs to the killer cell lectin-like receptor (KLR) family, which is a group of transmembrane proteins preferentially expressed in NK cells. Studies in mice suggested that the expression of this gene may be regulated by MHC class I molecules. Alternatively spliced transcript variants have been reported, but their full-length natures have not yet been determined.
killer cell lectin-like receptor subfamily G, member 1
, killer cell lectin-like receptor subfamily G member 1
, mast cell function-associated antigen 2F1
, C-type lectin domain family 15 member A
, C-type lectin domain family 15, member A
, ITIM-containing receptor MAFA-L
, MAFA-like receptor
, mast cell function-associated antigen (ITIM-containing)
, mast cell function-associated antigen