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cd45 leukocytes isolation kit miltenyi biotec  (Miltenyi Biotec)
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Cd45 Leukocytes Isolation Kit Miltenyi Biotec, supplied by Miltenyi Biotec, used in various techniques. Bioz Stars score: 97/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Disrupted cellular interaction network at the maternal–fetal interface in recurrent pregnancy loss (RPL). This schematic illustrates representative alterations in cell–cell communication associated with immune tolerance failure at the maternal–fetal interface. Under pathological conditions, impaired decidual stromal cell (DSC)-derived transforming growth factor-β (TGF-β) signaling may contribute to loss of the tolerogenic uterine natural killer (uNK) cell phenotype. Reduced Galectin-9 signaling and abnormal uNK–human <t>leukocyte</t> <t>antigen-C</t> <t>(HLA-C)/killer</t> <t>immunoglobulin-like</t> receptor (KIR) interactions may weaken trophoblast support. In parallel, macrophage polarization may shift toward a pro-inflammatory M1-like state, and the balance between regulatory T cells (Treg) and T helper 17 (Th17) cells may become disrupted. These alterations are associated with impaired trophoblast support and increased susceptibility to trophoblast stress and apoptosis. This figure is intended as a conceptual summary of reported cellular interaction abnormalities rather than a definitive mechanistic model. DSCs, decidual stromal cells; FASL, Fas ligand; HLA-C, human leukocyte antigen-C; KIR, killer cell immunoglobulin-like receptor; TGF-β, transforming growth factor-β; Th17, T helper 17 cells; TNFRs, tumor necrosis factor receptors; Treg, regulatory T cells; uNK, uterine natural killer cell.
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leukocyte differential  (Sysmex Corporation)
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Disrupted cellular interaction network at the maternal–fetal interface in recurrent pregnancy loss (RPL). This schematic illustrates representative alterations in cell–cell communication associated with immune tolerance failure at the maternal–fetal interface. Under pathological conditions, impaired decidual stromal cell (DSC)-derived transforming growth factor-β (TGF-β) signaling may contribute to loss of the tolerogenic uterine natural killer (uNK) cell phenotype. Reduced Galectin-9 signaling and abnormal uNK–human <t>leukocyte</t> <t>antigen-C</t> <t>(HLA-C)/killer</t> <t>immunoglobulin-like</t> receptor (KIR) interactions may weaken trophoblast support. In parallel, macrophage polarization may shift toward a pro-inflammatory M1-like state, and the balance between regulatory T cells (Treg) and T helper 17 (Th17) cells may become disrupted. These alterations are associated with impaired trophoblast support and increased susceptibility to trophoblast stress and apoptosis. This figure is intended as a conceptual summary of reported cellular interaction abnormalities rather than a definitive mechanistic model. DSCs, decidual stromal cells; FASL, Fas ligand; HLA-C, human leukocyte antigen-C; KIR, killer cell immunoglobulin-like receptor; TGF-β, transforming growth factor-β; Th17, T helper 17 cells; TNFRs, tumor necrosis factor receptors; Treg, regulatory T cells; uNK, uterine natural killer cell.
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Disrupted cellular interaction network at the maternal–fetal interface in recurrent pregnancy loss (RPL). This schematic illustrates representative alterations in cell–cell communication associated with immune tolerance failure at the maternal–fetal interface. Under pathological conditions, impaired decidual stromal cell (DSC)-derived transforming growth factor-β (TGF-β) signaling may contribute to loss of the tolerogenic uterine natural killer (uNK) cell phenotype. Reduced Galectin-9 signaling and abnormal uNK–human <t>leukocyte</t> <t>antigen-C</t> <t>(HLA-C)/killer</t> <t>immunoglobulin-like</t> receptor (KIR) interactions may weaken trophoblast support. In parallel, macrophage polarization may shift toward a pro-inflammatory M1-like state, and the balance between regulatory T cells (Treg) and T helper 17 (Th17) cells may become disrupted. These alterations are associated with impaired trophoblast support and increased susceptibility to trophoblast stress and apoptosis. This figure is intended as a conceptual summary of reported cellular interaction abnormalities rather than a definitive mechanistic model. DSCs, decidual stromal cells; FASL, Fas ligand; HLA-C, human leukocyte antigen-C; KIR, killer cell immunoglobulin-like receptor; TGF-β, transforming growth factor-β; Th17, T helper 17 cells; TNFRs, tumor necrosis factor receptors; Treg, regulatory T cells; uNK, uterine natural killer cell.
Leukocyte Acid Phosphatase Staining Kit, supplied by Servicebio Inc, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Disrupted cellular interaction network at the maternal–fetal interface in recurrent pregnancy loss (RPL). This schematic illustrates representative alterations in cell–cell communication associated with immune tolerance failure at the maternal–fetal interface. Under pathological conditions, impaired decidual stromal cell (DSC)-derived transforming growth factor-β (TGF-β) signaling may contribute to loss of the tolerogenic uterine natural killer (uNK) cell phenotype. Reduced Galectin-9 signaling and abnormal uNK–human <t>leukocyte</t> <t>antigen-C</t> <t>(HLA-C)/killer</t> <t>immunoglobulin-like</t> receptor (KIR) interactions may weaken trophoblast support. In parallel, macrophage polarization may shift toward a pro-inflammatory M1-like state, and the balance between regulatory T cells (Treg) and T helper 17 (Th17) cells may become disrupted. These alterations are associated with impaired trophoblast support and increased susceptibility to trophoblast stress and apoptosis. This figure is intended as a conceptual summary of reported cellular interaction abnormalities rather than a definitive mechanistic model. DSCs, decidual stromal cells; FASL, Fas ligand; HLA-C, human leukocyte antigen-C; KIR, killer cell immunoglobulin-like receptor; TGF-β, transforming growth factor-β; Th17, T helper 17 cells; TNFRs, tumor necrosis factor receptors; Treg, regulatory T cells; uNK, uterine natural killer cell.
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Disrupted cellular interaction network at the maternal–fetal interface in recurrent pregnancy loss (RPL). This schematic illustrates representative alterations in cell–cell communication associated with immune tolerance failure at the maternal–fetal interface. Under pathological conditions, impaired decidual stromal cell (DSC)-derived transforming growth factor-β (TGF-β) signaling may contribute to loss of the tolerogenic uterine natural killer (uNK) cell phenotype. Reduced Galectin-9 signaling and abnormal uNK–human <t>leukocyte</t> <t>antigen-C</t> <t>(HLA-C)/killer</t> <t>immunoglobulin-like</t> receptor (KIR) interactions may weaken trophoblast support. In parallel, macrophage polarization may shift toward a pro-inflammatory M1-like state, and the balance between regulatory T cells (Treg) and T helper 17 (Th17) cells may become disrupted. These alterations are associated with impaired trophoblast support and increased susceptibility to trophoblast stress and apoptosis. This figure is intended as a conceptual summary of reported cellular interaction abnormalities rather than a definitive mechanistic model. DSCs, decidual stromal cells; FASL, Fas ligand; HLA-C, human leukocyte antigen-C; KIR, killer cell immunoglobulin-like receptor; TGF-β, transforming growth factor-β; Th17, T helper 17 cells; TNFRs, tumor necrosis factor receptors; Treg, regulatory T cells; uNK, uterine natural killer cell.
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leukocytes subsets  (Miltenyi Biotec)
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Leukocyte populations dynamics in domestic pigs and wild boar infected with ASFV genotype II strain “Armenia 2007”. Statistically significant differences (means) between days after infection with respect to their pre-inoculation values were evaluated using the paired t-test. Black asterisks indicate statistically significant differences. Day post-infection (x-axis); Number of cells per mL (y-axis); WBC: white blood cells (total number of <t>leukocytes);</t> TD: termination day (euthanasia was performed once the humane endpoint was reached); Variables of significance (*p ≤ 0.05; **p ≤ 0.01; ***p ≤ 0.001).
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Leukocyte populations dynamics in domestic pigs and wild boar infected with ASFV genotype II strain “Armenia 2007”. Statistically significant differences (means) between days after infection with respect to their pre-inoculation values were evaluated using the paired t-test. Black asterisks indicate statistically significant differences. Day post-infection (x-axis); Number of cells per mL (y-axis); WBC: white blood cells (total number of <t>leukocytes);</t> TD: termination day (euthanasia was performed once the humane endpoint was reached); Variables of significance (*p ≤ 0.05; **p ≤ 0.01; ***p ≤ 0.001).
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Image Search Results


Disrupted cellular interaction network at the maternal–fetal interface in recurrent pregnancy loss (RPL). This schematic illustrates representative alterations in cell–cell communication associated with immune tolerance failure at the maternal–fetal interface. Under pathological conditions, impaired decidual stromal cell (DSC)-derived transforming growth factor-β (TGF-β) signaling may contribute to loss of the tolerogenic uterine natural killer (uNK) cell phenotype. Reduced Galectin-9 signaling and abnormal uNK–human leukocyte antigen-C (HLA-C)/killer immunoglobulin-like receptor (KIR) interactions may weaken trophoblast support. In parallel, macrophage polarization may shift toward a pro-inflammatory M1-like state, and the balance between regulatory T cells (Treg) and T helper 17 (Th17) cells may become disrupted. These alterations are associated with impaired trophoblast support and increased susceptibility to trophoblast stress and apoptosis. This figure is intended as a conceptual summary of reported cellular interaction abnormalities rather than a definitive mechanistic model. DSCs, decidual stromal cells; FASL, Fas ligand; HLA-C, human leukocyte antigen-C; KIR, killer cell immunoglobulin-like receptor; TGF-β, transforming growth factor-β; Th17, T helper 17 cells; TNFRs, tumor necrosis factor receptors; Treg, regulatory T cells; uNK, uterine natural killer cell.

Journal: Frontiers in Immunology

Article Title: Multi-omics insights into immune tolerance at the maternal–fetal interface in recurrent pregnancy loss: mechanisms, integration challenges, and translational perspectives

doi: 10.3389/fimmu.2026.1811970

Figure Lengend Snippet: Disrupted cellular interaction network at the maternal–fetal interface in recurrent pregnancy loss (RPL). This schematic illustrates representative alterations in cell–cell communication associated with immune tolerance failure at the maternal–fetal interface. Under pathological conditions, impaired decidual stromal cell (DSC)-derived transforming growth factor-β (TGF-β) signaling may contribute to loss of the tolerogenic uterine natural killer (uNK) cell phenotype. Reduced Galectin-9 signaling and abnormal uNK–human leukocyte antigen-C (HLA-C)/killer immunoglobulin-like receptor (KIR) interactions may weaken trophoblast support. In parallel, macrophage polarization may shift toward a pro-inflammatory M1-like state, and the balance between regulatory T cells (Treg) and T helper 17 (Th17) cells may become disrupted. These alterations are associated with impaired trophoblast support and increased susceptibility to trophoblast stress and apoptosis. This figure is intended as a conceptual summary of reported cellular interaction abnormalities rather than a definitive mechanistic model. DSCs, decidual stromal cells; FASL, Fas ligand; HLA-C, human leukocyte antigen-C; KIR, killer cell immunoglobulin-like receptor; TGF-β, transforming growth factor-β; Th17, T helper 17 cells; TNFRs, tumor necrosis factor receptors; Treg, regulatory T cells; uNK, uterine natural killer cell.

Article Snippet: Furthermore, abnormal uNK–trophoblast interactions have been associated with reduced Galectin-9 expression and imbalanced killer immunoglobulin-like receptor (KIR)–human leukocyte antigen-C (HLA-C) pairing, which may impair trophoblast invasiveness and endothelial remodeling, ultimately contributing to defective spiral artery remodeling and placental perfusion disorders ( , ).

Techniques: Derivative Assay

Leukocyte populations dynamics in domestic pigs and wild boar infected with ASFV genotype II strain “Armenia 2007”. Statistically significant differences (means) between days after infection with respect to their pre-inoculation values were evaluated using the paired t-test. Black asterisks indicate statistically significant differences. Day post-infection (x-axis); Number of cells per mL (y-axis); WBC: white blood cells (total number of leukocytes); TD: termination day (euthanasia was performed once the humane endpoint was reached); Variables of significance (*p ≤ 0.05; **p ≤ 0.01; ***p ≤ 0.001).

Journal: Frontiers in Immunology

Article Title: Dynamics of leukocyte populations, immune-regulatory cytokines, and biochemical parameters in wild boar and domestic pigs experimentally infected with a virulent African swine fever virus genotype II strain

doi: 10.3389/fimmu.2026.1751646

Figure Lengend Snippet: Leukocyte populations dynamics in domestic pigs and wild boar infected with ASFV genotype II strain “Armenia 2007”. Statistically significant differences (means) between days after infection with respect to their pre-inoculation values were evaluated using the paired t-test. Black asterisks indicate statistically significant differences. Day post-infection (x-axis); Number of cells per mL (y-axis); WBC: white blood cells (total number of leukocytes); TD: termination day (euthanasia was performed once the humane endpoint was reached); Variables of significance (*p ≤ 0.05; **p ≤ 0.01; ***p ≤ 0.001).

Article Snippet: The total number of leukocytes (WBC) and the main leukocytes subsets were evaluated by immunostaining with anti-CD45-FITC (Clone K252.1E4, Bio-Rad Antibodies, Kidlington, UK) and analyzed by flow cytometry using a MACSQuant, analyzer (Miltenyi Biotech, Bisley UK).

Techniques: Infection