# |
PMID |
Sentence |
1 |
28972490
|
Chronic lymphocytic leukaemia (CLL) is a lymphoproliferative disease characterised by accumulation of monoclonal CD19+CD5+CD23+ lymphocytes in the peripheral blood and bone marrow.
|
2 |
28972490
|
Phagocytic function was assessed through the ability of freshly isolated monocytes to attach and to engulf intact or opsonized Staphylococcus aureus particles in vitro with or without Granulocyte/Macrophage Colony Stimulating Factor (GM-CSF) and Interferon g (IFNg).
|
3 |
28972490
|
Simultaneously, immunophenotyping for FcγRI (CD64), FcγRII (CD32), FcγRIII (CD16) and CD180 has been carried out.
|
4 |
28972490
|
Our results demonstrated that phagocytosis of the intact and opsonised or intact S. aureus by monocytes of CLL patients was significantly decreased in comparison with normal controls, with no recovery upon the treatment with GM-CSF and IFNg.
|
5 |
28972490
|
A significant decrease in the expression of CD64 and CD180 has been detected on monocytes of CLL patients, with the drop in CD64 expression correlating with the disease progression and advanced Rai stages.
|
6 |
28972490
|
No appreciable changes were detected in the expression of CD32 and CD16 throughout the experiments.
|
7 |
28972490
|
The diminished expression of CD64 and CD180 provides possible explanation for the impaired phagocytic function of monocytes in CLL, as FcγRI receptor interaction with opsonising IgG1, and CD180 with the ligands on S. aureus might affect the ability of monocytes to attach and to engulf S. aureus particles and effectively eliminate the pathogen.
|
8 |
27742586
|
The intramuscular injection of an expression plasmid encoding turbot Ifng (pMCV1.4-ifng) was not able to affect the transcription of numerous immune genes directly related to the activity of IFN-gamma, with the exception of macrophage-colony stimulating factor (csf1).
|
9 |
27742586
|
On the other hand, some macrophage markers, such as the macrophage receptor with collagenous structure (marco), were down-regulated by Ifng during the viral infection.
|
10 |
26158463
|
In the present study, caprine MDMs were induced with LPS and ConA and the expression profile of immune response (IR) genes, namely, Tumor Necrosis Factor Alpha (TNFA), Interferon Gamma (IFNG), Interleukin 2 (IL2), Granulocyte Macrophage Colony Stimulating Factor (GMCSF), Interleukin 10 (IL10), Transforming Growth Factor Beta (TGFB), Natural Resistance-Associated Macrophage Protein-1 (NRAMP1), inducible nitric oxide synthase (NOS2), and caspase1 (CASP1) were studied to compare the potential of LPS and ConA in initiating immune responses in goat macrophages.
|
11 |
26158463
|
Real Time quantitative PCR (RT-qPCR) analysis revealed that both LPS and ConA caused an upregulation (p < 0.05) of GMCSF, TGFB1, IL10, and IFNG and down-regulation of NRAMP1.
|
12 |
26158463
|
TNFA and IL2, and NOS2 were upregulated (p < 0.05) by ConA and LPS, respectively.
|
13 |
25965835
|
These included cadherin 13 (Cdh13), colony stimulating factor 1 (Csf1), chemokine C-X-C motif ligand 1 (Cxcl1), endothelial cell-selective adhesion molecule (Esam), and interferon gamma (Ifng).
|
14 |
25956299
|
The balance between survival agents, including GM-CSF, CSF1, LIF, HB-EGF and IGFII, against apoptosis-inducing factors such as TNFα, TRAIL and IFNg, influence the course of preimplantation development, causing embryos to develop normally, adapt to varying maternal environments, or in some cases to arrest and undergo demise.
|
15 |
25496030
|
This phase I/II study assessed the safety, immunity and clinical response to 6 or 12 bi-weekly intradermal ImMucin vaccines, co-administered with human granulocyte-macrophage colony-stimulating factor to 15 MUC1-positive multiple myeloma (MM) patients, with residual or biochemically progressive disease following autologous stem cell transplantation.
|
16 |
25496030
|
ImMucin vaccination induced a robust increase in γ-interferon (IFN-γ-producing CD4+ and CD8+ T-cells (≤80-fold), a pronounced population of ImMucin multimer CD8+ T-cells (>2%), a 9·4-fold increase in peripheral blood mononuclear cells proliferation and 6·8-fold increase in anti-ImMucin antibodies, accompanied with T-cell and antibody-dependent cell-mediated cytotoxicity.
|
17 |
25138705
|
The cytokines that were found to fluctuate over the course of the oestrous cycle were colony-stimulating factor (CSF)1, CSF2, interferon gamma (IFNG) and tumour necrosis factor alpha (TNFA), all of which were significantly elevated at oestrus compared with other phases.
|
18 |
25138705
|
The cytokines that were found to fluctuate over the course of the oestrous cycle were colony-stimulating factor (CSF)1, CSF2, interferon gamma (IFNG) and tumour necrosis factor alpha (TNFA), all of which were significantly elevated at oestrus compared with other phases.
|
19 |
25138705
|
The concentration of serum progesterone during the oestrus phase negatively correlated with the abundance of cytokines CSF3, IL12p40, IFNG and leukaemia inhibitory factor (LIF).
|
20 |
25138705
|
The concentration of serum progesterone during the oestrus phase negatively correlated with the abundance of cytokines CSF3, IL12p40, IFNG and leukaemia inhibitory factor (LIF).
|
21 |
25138705
|
In ovariectomised mice, exogenous oestradiol administration increased mammary gland CSF1, CSF2, IFNG and LIF, compared with ovariectomised control mice.
|
22 |
25138705
|
In ovariectomised mice, exogenous oestradiol administration increased mammary gland CSF1, CSF2, IFNG and LIF, compared with ovariectomised control mice.
|
23 |
25138705
|
Progesterone administration together with oestradiol resulted in reduced CSF1, CSF3 and IFNG compared with oestradiol administration alone.
|
24 |
25138705
|
Progesterone administration together with oestradiol resulted in reduced CSF1, CSF3 and IFNG compared with oestradiol administration alone.
|
25 |
23566200
|
Mϕs differentiated with macrophage colony-stimulating factor and interferon-γ (Mγ-Mϕs), which are similar to the human intestinal lamina propria CD14(+) Mϕs that contribute to Crohn's disease (CD) pathogenesis by production of pro-inflammatory cytokines, highly expressed TGR5 compared with any other type of differentiated Mϕ and dendritic cells.
|
26 |
23566200
|
Among LPMCs, isolated CD14(+) intestinal Mϕs from patients with CD expressed TGR5.
|
27 |
23566200
|
In isolated intestinal CD14(+) Mϕs, a TGR5 agonist could inhibit tumour necrosis factor-α production.
|
28 |
18653623
|
Insulin-like growth factor-1 delays Fas-mediated apoptosis in human neutrophils through the phosphatidylinositol-3 kinase pathway.
|
29 |
18653623
|
We previously showed that insulin-like growth factor-1 (IGF1) delays spontaneous neutrophil apoptosis without influencing the secretion of cytokines by these cells.
|
30 |
18653623
|
We show that IGF1 delays neutrophil apoptosis triggered by the agonistic anti-Fas antibody CH11 and that the effect of IGF1 is comparable in magnitude to that of the acknowledged anti-apoptotic cytokines interferon-gamma (IFNG) and granulocyte-macrophage colony-stimulating factor (GM-CSF; now known as CSF2).
|
31 |
18653623
|
IGF1 did not affect Fas expression or activation by anti-Fas of caspase-8, but inhibited the depolarization of the mitochondrial membrane.
|
32 |
18653623
|
Inhibitor studies indicate that the phosphatidylinositol-3 kinase (PI3K) pathway, but not the MEK-ERK pathway, mediates the effects of IGF1.
|
33 |
18653623
|
However, in contrast to CSF2, IGF1 did not induce phosphorylation and translocation to the membrane of AKT, the canonical downstream target of PI3K.
|
34 |
18653623
|
We therefore speculate that other downstream targets of PI3K are involved in the delay of neutrophil apoptosis by IGF1, possibly through stabilization of the mitochondrial membrane.
|
35 |
19578489
|
We identified 7 proteins that significantly differentiate HCC patients from hepatitis patients (p < 0.05) (AFP, CTNNB, CSF1, SELL, IGFBP6, IL6R, and VCAM1).
|
36 |
19578489
|
Importantly, we also identified 8 proteins that significantly differentiate HCC patients with 'normal' levels of AFP (< 20 ng/ml) from hepatitis patients (p < 0.05) (IL1RN, IFNG, CDKN1A, RETN, CXCL14, CTNNB, FGF2, and SELL).
|
37 |
18006399
|
Gene expression of RANKL, OPG, TGFB2, IFNG and CSF-1 was analyzed after no mechanical stimulation (control), exposure to compression or exposure to micromotions.
|
38 |
18006399
|
We observed an 8-fold upregulation of RANKL after exposure to micromotions, and downregulation of OPG, IFNG and TGFB2.
|
39 |
18006399
|
The RANKL:OPG ratio was upregulated 24-fold after micromotions.
|