scholarly journals Decidual vascular endothelial cells promote maternal–fetal immune tolerance by inducing regulatory T cells through canonical Notch1 signaling

2017 ◽  
Vol 95 (4) ◽  
pp. 416-416
Author(s):  
Yanyi Yao ◽  
Jieping Song ◽  
Weipeng Wang ◽  
Nian Liu
Keyword(s):  
T Cells ◽  
Endothelial Cells ◽  
Regulatory T Cells ◽  
Immune Tolerance ◽  
Vascular Endothelial Cells ◽  
Vascular Endothelial ◽  
Notch1 Signaling

scholarly journals The human OX40/gp34 system directly mediates adhesion of activated T cells to vascular endothelial cells.

1996 ◽  
Vol 183 (5) ◽  
pp. 2185-2195 ◽  
Author(s):  
A Imura ◽  
T Hori ◽  
K Imada ◽  
T Ishikawa ◽  
Y Tanaka ◽  
...  
Keyword(s):  
T Cells ◽  
Endothelial Cells ◽  
T Cell ◽  
Cell Line ◽  
Cell Lines ◽  
Vascular Endothelial Cells ◽  
Vascular Endothelial ◽  
Cell Leukemia ◽  
Activated T Cells ◽  
T Cell Lines

Fresh leukemic cells from patients with adult T cell leukemia (ATL) and some ATL-derived T cell lines show adhesion to human umbilical vein endothelial cells (HUVECs) mainly through E-selectin, but a proportion of this binding remains unaffected by the addition of combinations of antibodies against known adhesion molecules. By immunizing mice with one of such cell lines, we established monoclonal antibodies (mAbs), termed 131 and 315, that recognize a single cell surface antigen (Ag) and inhibit the remaining pathway of the adhesion. These mAbs did not react with normal resting peripheral blood mononuclear cells (PBMC) or most of the cell lines tested except for two other human T cell leukemia virus type I (HTLV-I)-infected T cell lines. After stimulation with phytohemagglutinin (PHA), PBMC expressed Ag 131/315 transiently, indicating that these mAbs define a T cell activation Ag. Western blotting and immunoprecipitation revealed that Ag 131/315 has an apparent molecular mass of 50 kD. Expression cloning was done by transient expression in COS-7 cells and immunological selection to isolate a cDNA clone encoding Ag 131/315. Sequence analysis of the cDNA indicated that it is identical to human OX40, a member of the tumor necrosis factor/nerve growth factor receptor family. We then found that gp34, the ligand of OX40, was expressed on HUVECs and other types of vascular endothelial cells. Furthermore, it was shown that the adhesion of CD4+ cells of PHA-stimulated PBMC to unstimulated HUVECs was considerably inhibited by either 131 or 315. Finally, OX40 transfectants of Kit 225, a human interleukin 2-dependent T cell line, were bound specifically to gp34 transfectants of MMCE, a mouse epithelial cell line, and this binding was blocked by either 315 or 5A8, an anti-gp34 mAb. These results indicate that the OX40/gp34 system directly mediates adhesion of activated T cells or OX40+-transformed T cells to vascular endothelial cells.

scholarly journals Expression of functional CD40 by vascular endothelial cells.

1995 ◽  
Vol 182 (1) ◽  
pp. 33-40 ◽  
Author(s):  
D Hollenbaugh ◽  
N Mischel-Petty ◽  
C P Edwards ◽  
J C Simon ◽  
R W Denfeld ◽  
...  
Keyword(s):  
T Cells ◽  
Endothelial Cells ◽  
Adhesion Molecule ◽  
Inflammatory Disease ◽  
Vascular Endothelium ◽  
Cell Activation ◽  
Inflammatory Responses ◽  
Vascular Endothelial Cells ◽  
Intercellular Adhesion Molecule ◽  
Vascular Endothelial

The interaction between activated vascular endothelium and T cells has been shown to play an important role in the recruitment and activation of T cells at sites of inflammation. Here we report the expression of CD40 by vascular endothelial cells and its regulation by inflammatory agents. Using the soluble recombinant CD40 ligand, sgp39, we show that the interaction of CD40 with its ligand can lead to endothelial cell activation, which in turn leads to leukocyte adhesion. This adhesion is partly mediated by the expression of E-selectin. In addition to E-selectin expression, sgp39 induces the expression of intercellular adhesion molecule 1 and augments the tumor necrosis factor alpha-induced expression of vascular cell adhesion molecule 1. The effects of sgp39 on endothelial cells can be blocked with anti-gp39 monoclonal antibody (mAb), anti-CD40 mAb, or soluble CD40. Staining of tissues from healthy human skin using anti-CD40 mAb showed very weak expression of CD40 by the endothelium, while skin involved in inflammatory disease showed marked upregulation of CD40 expression. These studies suggest that interactions between cell surface proteins expressed by activated T cells with their receptors on vascular endothelium can stimulate the vasculature at sites of inflammation and may be involved in normal inflammatory responses and in inflammatory disease.

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