scholarly journals Human endothelial cell-lymphocyte interaction. Endothelial cells function as accessory cells necessary for mitogen-induced human T lymphocyte activation in vitro.

1981 ◽  
Vol 67 (5) ◽  
pp. 1490-1499 ◽  
Author(s):  
E R Ashida ◽  
A R Johnson ◽  
P E Lipsky
Keyword(s):  
Endothelial Cells ◽  
Endothelial Cell ◽  
T Lymphocyte ◽  
Lymphocyte Activation ◽  
Human Endothelial Cell ◽  
T Lymphocyte Activation ◽  
Accessory Cells ◽  
Human T Lymphocyte

T LYMPHOCYTE ACTIVATION BY CYTOMEGALOVIRUS-INFECTED, ALLOGENEIC CULTURED HUMAN ENDOTHELIAL CELLS

1992 ◽  
Vol 54 (5) ◽  
pp. 887-895 ◽  
Author(s):  
W. James Waldman ◽  
Patrick W. Adams ◽  
Charles G. Orosz ◽  
Daniel D. Sedmak
Keyword(s):  
Endothelial Cells ◽  
T Lymphocyte ◽  
Lymphocyte Activation ◽  
Human Endothelial Cells ◽  
T Lymphocyte Activation

Induction of endothelial proliferation and angiogenesis through activating the ERK1/2/EGF pathway mediate by CXC chemokine receptor 2 by chemokine (C-X-C motif) ligand 1.

2013 ◽  
Vol 31 (6_suppl) ◽  
pp. 138-138 ◽  
Author(s):  
Makito Miyake ◽  
Steve Goodison ◽  
Evan Gomes ◽  
Wasia Rizwani ◽  
Shanti Ross ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Endothelial Cells ◽  
Endothelial Cell ◽  
Chemokine Receptor ◽  
Cellular Proliferation ◽  
Human Endothelial Cell ◽  
Endothelial Cell Proliferation ◽  
Cxc Chemokine ◽  
Inhibition Of Angiogenesis

138 Background: Endothelial cell growth and proliferation are critical for tumoral angiogenesis. We report here that blockade of Chemokine (C-X-C motif) ligand 1 (CXCL1) results in reduction of human endothelial cell proliferation and its ability to induce angiogenesis. Methods: Two human endothelial cell lines, HUVEC and HDMEC, were used in the in vitro assays. Proliferation assay and matrigel tube formation assay were performed to test the inhibitory effect of anti-CXCL antibody on the activity of endothelial cells in vitro. Matrigel plug assay in nude mice was performed to test the in vivo angiogenic activity of CXCL1. Results: CXCL1 interacts with its receptor CXC chemokine Receptor 2 and induces endothelial cell proliferation, whereas blockade of CXCL1 is associated with reduction in cellular proliferation through a decrease in levels of cyclin D and cdk4 and inhibition of angiogenesis through EGF and ERK 1/2. Targeting CXCL1 inhibits neoangiogenesis but has no effect on disrupting established vasculature. Furthermore targeting CXCL1 is associated with reduction in migration of human endothelial cells in an in vitro model. Additionally, neutralizing antibody against CXCL1 in a xenograft angiogenesis model resulted in inhibition of angiogenesis. Conclusions: CXCL1-induced regulation of angiogenesis has not been studied extensively in human cancers, thus these findings illustrate a novel contribution of CXCL1 interactions in pathological angiogenesis. Therefore, the ability to selectively modulate CXCL1, specifically in tumoral angiogenesis, may promote the development of novel oncologic therapeutic strategies.

scholarly journals Human plasma-like medium improves T lymphocyte activation

2019 ◽  
Author(s):  
Michael A. Leney-Greene ◽  
Arun K. Boddapati ◽  
Helen C. Su ◽  
Jason Cantor ◽  
Michael J. Lenardo
Keyword(s):  
Human Plasma ◽  
T Cell Activation ◽  
T Lymphocyte ◽  
Cell Activation ◽  
Lymphocyte Activation ◽  
Cell Physiology ◽  
Transcriptional Responses ◽  
T Lymphocyte Activation ◽  
Synthetic Media

SUMMARYT lymphocytes are critical for effective immunity and the ability to study their behavior in synthetic media in vitro facilitates major discoveries in their development, function, and fate. However, the composition of human plasma differs from synthetic media and we hypothesized that these differences could have important effects on cell physiology. We therefore compared T lymphocyte activation in human plasma-like medium (HPLM) to RPMI supplemented with dialyzed FBS (RPMIdFBS) and found that it entrained markedly different transcriptional responses. We also found that the concentration of calcium in RPMIdFBS is six-fold lower than HPLM causing altered T cell activation which could be reversed by calcium addition. Thus, investigators should be cognizant of differences between commonly used media formulations and HPLM which is based on the in vivo plasma environment as these could profoundly affect their experimental results. Physiologic media may be a valuable new way to study immune cells in culture.

Suppression of T lymphocyte activation by 3-chloro-1,2-propanediol mono- and di-palmitate esters in vitro

2018 ◽  
Vol 51 ◽  
pp. 54-62 ◽  
Author(s):  
Guoren Huang ◽  
Jinli Xue ◽  
Xiangjun Sun ◽  
Jing Wang ◽  
Yilin Wang ◽  
...  
Keyword(s):  
T Lymphocyte ◽  
Lymphocyte Activation ◽  
T Lymphocyte Activation

scholarly journals Toll-like receptor 4 inhibition prevents autoimmune diabetes in NOD mice

2019 ◽  
Vol 9 (1) ◽  
Author(s):  
Mohamed Alibashe-Ahmed ◽  
Estelle Brioudes ◽  
Walter Reith ◽  
Domenico Bosco ◽  
Thierry Berney
Keyword(s):  
T Lymphocyte ◽  
Autoimmune Diabetes ◽  
Lymphocyte Activation ◽  
Nod Mice ◽  
Diabetes Incidence ◽  
Preventive Strategy ◽  
Tlr4 Signaling ◽  
T Lymphocyte Activation ◽  
And Control

AbstractTLR4 is a transmembrane receptor of the innate immune system that recognizes LPS from gram-negative bacteria. Its stimulation induces pro-inflammatory responses and modulates adaptive immunity. Our aim is to determine the role of TLR4 in the activation and proliferation of T lymphocytes in the onset of autoimmune diabetes, using the non-obese diabetic (NOD) mouse model. Antigen-specific activation and proliferation of diabetogenic T cells were assessed in vitro by Carboxyfluorescein succinimidyl ester (CFSE) dilution, in presence of vehicle or CLI-095, a cyclohexene derivative that inhibits TLR4 signaling. NOD mice were treated with vehicle or CLI-095 and sacrificed either before or after the onset of autoimmune diabetes. T lymphocyte activation and proliferation were evaluated in treated and control mice. Insulitis was analyzed by histology and diabetes incidence was determined in treated and control mice. Our results demonstrate that TLR4 blockade decreases CD4+ T lymphocyte activation and auto-antigen-specific proliferation both in vitro and in vivo, decreases the infiltrative insulitis and finally prevents the onset of spontaneous diabetes. Taken together, our data demonstrate that TLR4 signaling contributes to the development and maintenance of autoimmune diabetes. The immunomodulatory effect of CLI-095 could be part of a preventive strategy targeting patients at risk for type 1 diabetes.

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