Objective: To investigatethe expressions of NKG2A, NKG2C receptors and their ligand HLA-E in decidua of preeclampsia patients.
Methods: Decidua tissues were collected from 30 patients with mild preeclampsia, 42 patients with severe preeclampsia and 46 normal pregnancy as contrast. The expressions of NKG2A, NKG2C protein were detected by immunohistochemitry and mRNAs of NKG2A, NKG2C and HLA-E genes were detected by RT-PCR.
Results: The expression of HLA-E mRNA was significantly decreased in preeclampsia, especially in severe preeclampsia patients (P < 0.05); The mRNA and protein expression of NKG2A, NKG2C in severe preeclampsia group were significantly higher than that in normal pregnancy group (P < 0.05); In the severe preeclampsia group, the ratio of expression level of NKG2A and NKG2C was significantly lower than that of normal group and the mRNA and protein expression of NKG2C receptor were both significantly higher than that of NKG2A (P < 0.05); The mRNA expression level of HLA-E, NKG2A and NKG2C were closely related with clinical and biochemical indexes,such as blood pressure of late pregnancy and 24-hour proteinuria.
Conclusion: The decreased expression of HLA-E and the unevenly increase of NKG2A and NKG2C may involve in the pathogenesis of preeclampsia.
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Transplant Cell Ther
January 2025
Division of Clinical Research, Fred Hutchinson Cancer Center, Seattle, Washington.
Background: Recurrence of blood malignancy is the major cause of mortality after hematopoietic cell transplantation. NKG2 receptor/HLA-E ligand complexes play a fundamental role in the surveillance and elimination of transformed cells but their role in the control of leukemia in transplantation is unknown.
Objective: We tested the hypothesis that gene variation of patient and/or donor HLA-E ligand and donor NKG2C-NKG2A receptors are associated with the risks of relapse and mortality (primary endpoints) and GVHD and non-relapse mortality (secondary endpoints) after haploidentical transplantation.
Infect Immun
December 2024
Institute for Medical Microbiology and Hygiene, University Hospital Ulm, Ulm, Germany.
Protection against infections with intracellular bacteria requires the interaction of macrophages and T-lymphocytes, including CD8 T cells. Recently, the expression of natural killer cell receptors NKG2A and NKG2C was introduced as markers of CD8 T-cell subsets. The goal of this study was to functionally characterize human NKG2A and NKG2C-expressing T cells using the major pathogen () as a model organism.
View Article and Find Full Text PDFAntibodies (Basel)
November 2024
BioRay Pharmaceutical Co., Ltd., Taizhou 318000, China.
Immuno-oncology has revolutionized cancer treatment, with NKG2A emerging as a novel target for immunotherapy. The blockade of NKG2A using the immune checkpoint inhibitor (ICI) monalizumab has been shown to enhance the responses of both NK cells and CD8+ T cells. However, monalizumab has demonstrated limited efficacy in in vitro cytotoxic assays and clinical trials.
View Article and Find Full Text PDFHLA
November 2024
Immunogenetics & Histocompatibility Lab, Instituto de Investigación Sanitaria Puerta de Hierro - Segovia de Arana, Majadahonda, Spain.
A subpopulation of NK cells with distinctive phenotype and function differentiates and expands specifically in response to infection by human cytomegalovirus (HCMV). A hallmark of these adaptive NK cells is their increased expression levels of the activating CD94/NKG2C receptor for HLA-E, and lack of expression of its inhibitory homologue CD94/NKG2A. Their frequency is highly variable in HCMV individuals, and the basis for such differences is only partially understood.
View Article and Find Full Text PDFFront Immunol
November 2024
Núcleo de Doenças Infecciosas, Universidade Federal do Espírito Santo, Vitória, Brazil.
Cytotoxic activity is a hallmark of the immunopathogenesis in human cutaneous leishmaniasis (CL). In this study, we identified accumulation of CD4 granzyme B producing T cells with increased cytotoxic capacity in CL lesions. These cells showed enhanced expression of activating NK receptors (NKG2D and NKG2C), diminished expression of inhibitory NKG2A, along with the upregulation of the senescence marker CD57.
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