scholarly journals Tbet promotes CXCR6 expression in immature natural killer cells and natural killer cell egress from the bone marrow

Immunology ◽  
2020 ◽  
Vol 161 (1) ◽  
pp. 28-38
Author(s):  
Antonia O. Cuff ◽  
Thibaut Perchet ◽  
Simone Dertschnig ◽  
Rachel Golub ◽  
Victoria Male
Keyword(s):  
Bone Marrow ◽  
Natural Killer Cells ◽  
Natural Killer Cell ◽  
Natural Killer ◽  
Killer Cell ◽  
Killer Cells

Molecular basis of human natural killer cell recognition of HLA-E (human leucocyte antigen-E) and its relevance to clearance of pathogen-infected and tumour cells

2000 ◽  
Vol 99 (1) ◽  
pp. 9-17 ◽  
Author(s):  
Christopher A. O'CALLAGHAN
Keyword(s):  
Endoplasmic Reticulum ◽  
Natural Killer Cells ◽  
Natural Killer Cell ◽  
Cell Surface ◽  
Natural Killer ◽  
Human Leucocyte Antigen ◽  
Killer Cell ◽  
Tumour Cells ◽  
Leader Peptide ◽  
Killer Cells

HLA-E (human leucocyte antigen-E) is a conserved class I major histocompatibility molecule which has only limited polymorphism. It binds to the leader peptide derived from the polymorphic classical major histocompatibility molecules HLA-A, HLA-B and HLA-C. This peptide binding is highly specific and stabilizes the HLA-E protein, allowing it to migrate to the cell surface. A functioning TAP (transporter associated with antigen processing) molecule is required to transport these peptides into the endoplasmic reticulum, where they can interact with HLA-E. HLA-E then migrates to the cell surface, where it interacts with CD94/NKG2A receptors on natural killer cells. This interaction inhibits natural killer cell-mediated lysis of a cell displaying HLA-E. If the leader peptide is not present in the endoplasmic reticulum, HLA-E is unstable and is degraded before it reaches the cell surface. In damaged cells, such as virally infected or tumour cells, down-regulation of HLA-A, HLA-B and HLA-C production or inhibition of TAP prevents stabilization of HLA-E by the leader peptide. Under these circumstances, HLA-E does not reach the cell surface and the cell is then vulnerable to lysis by natural killer cells. The molecular mechanisms underlying this function of HLA-E have been revealed by crystallographic studies of the structure of HLA-E.

scholarly journals Frequency and phenotype of natural killer cells and natural killer cell subsets in bovine lymphoid compartments and blood

Immunology ◽  
2017 ◽  
Vol 151 (1) ◽  
pp. 89-97 ◽  
Author(s):  
Carly A. Hamilton ◽  
Suman Mahan ◽  
Charlotte R. Bell ◽  
Bernardo Villarreal-Ramos ◽  
Bryan Charleston ◽  
...  
Keyword(s):  
Natural Killer Cells ◽  
Natural Killer Cell ◽  
Natural Killer ◽  
Killer Cell ◽  
Killer Cells

scholarly journals Reduced proportion and activity of natural killer cells in patients with Graves’ disease

2020 ◽  
Vol 18 ◽  
pp. 205873922094233
Author(s):  
Qingqing Yang ◽  
Li Zhang ◽  
Cheng Guo ◽  
ChunJia Kou ◽  
Yu Long ◽  
...  
Keyword(s):  
Natural Killer Cells ◽  
Natural Killer Cell ◽  
Natural Killer ◽  
Killer Cell ◽  
Graves Disease ◽  
Newly Diagnosed ◽  
Free Triiodothyronine ◽  
Killer Cells ◽  
Kir Genes ◽  
The Difference

Natural killer cells not only play important roles in protecting against viral infection and cancer but also involved in the pathogenesis of Graves’ disease. Killer Ig-like receptor (KIR) genes encode receptors which are mostly expressed on and regulate the activation of natural killer cells. Our previous research found that the KIR2DS4 gene frequency was lower in patients with Graves’ disease than in controls. Nevertheless, the specific mechanisms by which natural killer cell act is obscure in Graves’ disease. In total, 178 participants including newly diagnosed Graves’ disease patients (n = 95) and healthy individuals (n = 83) were recruited in this study. TSH (thyrotropin), FT3 (free triiodothyronine), and FT4 (free thyroxine) were assayed using electro chemiluminescent immunoassays. The counts of natural killer cell (CD3−CD56+ natural killer cell), activated natural killer cell (CD3−CD56+CD69+ natural killer cell), and KIR2DS4-expressing natural killer cell (CD3−CD56+CD158i+ natural killer cell) in peripheral blood were analyzed using flow cytometry. The proportions of natural killer cells and activated natural killer cells were lower in the newly diagnosed Graves’ disease patients than in the controls; the difference was statistically significant ( P < 0.05). However, the difference in the proportion of KIR2DS4-expressing natural killer cells between the two groups was not statistically significant. In Graves’ disease patients, no relationship was found between the proportion of natural killer cells and the blood FT3 level, the blood FT4 level, or the blood TSH level; however, the proportion of activated natural killer cells was negatively correlated with FT3 and FT4 and positively correlated with TSH. Our research findings revealed that a reduction in the counts of natural killer cell and activated natural killer cell might be involved in Graves’ disease pathogenesis.

scholarly journals Natural Killer Cell Counts Are Not Different between Patients with Post-Lyme Disease Syndrome and Controls

2009 ◽  
Vol 16 (8) ◽  
pp. 1249-1250 ◽  
Author(s):  
Adriana Marques ◽  
Margaret R. Brown ◽  
Thomas A. Fleisher
Keyword(s):  
Natural Killer Cells ◽  
Lyme Disease ◽  
Natural Killer Cell ◽  
Healthy Volunteers ◽  
Natural Killer ◽  
Killer Cell ◽  
Killer Cells ◽  
Chronic Lyme Disease ◽  
Cell Counts

ABSTRACT It has been reported that patients with “chronic Lyme disease” have a decreased number of natural killer cells, as defined by the CD57 marker. We performed immunophenotyping in 9 individuals with post-Lyme disease syndrome, 12 who recovered from Lyme disease, and 9 healthy volunteers. The number of natural killer cells was not significantly different between the groups.

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