scholarly journals HSD11B1 is upregulated synergistically by IFNγ and TNFα and mediates TSG-6 expression in human UC-MSCs

2020 ◽  
Vol 6 (1) ◽  
Author(s):  
Peiqing Huang ◽  
Yinghong Li ◽  
Chenchang Xu ◽  
Gerry Melino ◽  
Changshun Shao ◽  
...  
Keyword(s):  
2012 ◽  
Vol 2012 ◽  
pp. 1-10 ◽  
Author(s):  
Raj Raghupathy ◽  
Majedah Al-Azemi ◽  
Fawaz Azizieh

Intrauterine growth restriction (IUGR) is an important perinatal syndrome that poses several serious short- and long-term effects. We studied cytokine production by maternal peripheral blood lymphocytes stimulated by trophoblast antigens. 36 women with a diagnosis of IUGR and 22 healthy women with normal fetal growth were inducted. Peripheral blood mononuclear cells were stimulated with trophoblast antigens and levels of the proinflammatory cytokines IL-6, IL-8, IL-12, IL-23, IFNγ, and TNFα and the anti-inflammatory cytokines IL-4, IL-10, and IL-13 were measured in culture supernatants by ELISA. IL-8 was produced at higher levels by blood cells of the IUGR group than normal pregnant women, while IL-13 was produced at lower levels. IL-8, IFNγ, and TNFα were higher in IUGR with placental insufficiency than in normal pregnancy. IL-12 levels were higher and IL-10 levels were lower in IUGR with placental insufficiency than in IUGR without placental insufficiency. We suggest that a stronger pro-inflammatory bias exists in IUGR as compared to normal pregnancy and in IUGR with placental insufficiency when compared to IUGR without placental insufficiency. Several ratios of proinflammatory to anti-inflammatory cytokines also support the existence of an inflammatory bias in IUGR.


2010 ◽  
Vol 29 (2) ◽  
pp. S101-S101
Author(s):  
C.-L. Liew ◽  
G. Hodge ◽  
S. Hodge ◽  
D. Chambers ◽  
P. Hopkins ◽  
...  
Keyword(s):  
T Cell ◽  

1997 ◽  
Vol 108 (1) ◽  
pp. 62-67 ◽  
Author(s):  
Tadashi Terui ◽  
Kuniaki Ishii ◽  
Maki Ozawa ◽  
Nobuko Tabata ◽  
Taizo Kato ◽  
...  

2019 ◽  
Vol 10 (1) ◽  
Author(s):  
Xiaolei Li ◽  
Bingxue Shang ◽  
Ya-nan Li ◽  
Yufang Shi ◽  
Changshun Shao

Blood ◽  
2010 ◽  
Vol 116 (21) ◽  
pp. 4532-4532
Author(s):  
Mette Hoegh-Petersen ◽  
Lina Roa ◽  
Yiping Liu ◽  
Feng Zhou ◽  
Alejandra Ugarte-Torres ◽  
...  

Abstract Abstract 4532 Background. Cytomegalovirus (CMV) reactivates (becomes detectable in blood) in most seropositive hematopoietic cell transplant (HCT) recipients. In some reactivating patients, low level viremia (<50,000 DNA copies/ml plasma, ie, less than our institutional threshold for preemtive therapy) progresses to high level viremia or CMV disease, which is potentially fatal. We hypothesized that low level viremia progresses in patients with low specific T cell counts and spontaneously resolves in patients with high specific T cell counts. Methods. In 30 CMV seropositive HCT recipients monitored weekly for reactivation by real-time PCR, blood was drawn for specific T cell counts within 4 days from the first episode of low level viremia. Fourteen patients received grafts from seropositive donors (D+R+), and 16 patients from seronegative donors (D-R+). Mononuclear cells were stimulated overnight with CMV lysate, pp65 overlapping peptides, no stimulus (negative control) or staphylococcal enterotoxin B (positive control). T cells producing IFNγ, TNFα and/or IL2 were enumerated by flow cytometry. Results. Among D+R+ patients, counts of CMV lysate and pp65 specific CD4 T cells producing IFNγ and TNFα (and not IL2) were higher in patients with spontaneous resolution than patients with progression (p=0.02 for CMV lysate, p=0.004 for pp65). Also, there was an inverse correlation between pp65 specific CD8 T cells producing IFNγ and TNFα and peak viremia (r=-0.94, p=0.005) in D+R+ patients who progressed to high level viremia/disease. In contrast, among D-R+ patients, CMV lysate and pp65 specific T cell counts were similar in patients with spontaneous resolution and patients with progression, and there was no correlation between specific T cell counts and peak viremia. Conclusion. CMV specific T cells play a role in preventing progression from low to high level CMV reactivation/disease in D+R+ patients. Other immune mechanisms (eg, NK cells?) play the role in D-R+ patients. Disclosures: No relevant conflicts of interest to declare.


1992 ◽  
Vol 34 (1) ◽  
pp. 29
Author(s):  
M. Carreno ◽  
L. Fuller ◽  
K. Zucker ◽  
D. Asthana ◽  
J. Fernandez ◽  
...  

2012 ◽  
Vol 213 (2) ◽  
pp. 183-191 ◽  
Author(s):  
Alessandro Antonelli ◽  
Silvia Martina Ferrari ◽  
Silvia Frascerra ◽  
Ilaria Ruffilli ◽  
Cinzia Pupilli ◽  
...  

No data are present in the literature about the effect of cytokines on the prototype β chemokine (C-C motif) ligand 2 (CCL2) or of peroxisome proliferator-activated receptor α (PPARα (PPARA)) activation on CCL2 and CXCL10 chemokines secretion in fibroblasts or preadipocytes in Graves' ophthalmopathy (GO). We have tested the effect of interferon γ (IFNγ (IFNG)) and tumor necrosis factor α (TNFα) on CCL2, and for comparison on the prototype α chemokine (C-X-C motif) ligand 10 (CXCL10), and the possible modulatory role of PPARα activation on secretion of these chemokines in normal and GO fibroblasts or preadipocytes in primary cell cultures. This study shows that IFNγ alone, or in combination with TNFα, stimulates the secretion of CCL2 in primary orbital fibroblasts or preadipocytes from patients with GO at levels similar to those observed in controls. IFNγ and TNFα also stimulated CXCL10 chemokine secretion as expected. The presence of PPARα and PPARγ (PPARG) in primary fibroblasts or preadipocytes of patients with GO has been confirmed. PPARα activators were able to inhibit the secretion of CXCL10 and CCL2, while PPARγ activators were confirmed to be able to inhibit CXCL10 but had no effect on CCL2. PPARα activators were stronger inhibitors of chemokine secretions than PPARγ agonists. In conclusion, CCL2 and CXCL10 are modulated by IFNγ and TNFα in GO. PPARα activators inhibit the secretion of the main prototype α (CXCL10) and β (CCL2) chemokines in GO fibroblasts or preadipocytes, suggesting that PPARα may be involved in the modulation of the immune response in GO.


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