Interactions between endothelial cells and alloreactive T cells involved in allograft immunity. Bernd Markus, Yolonda Colson, John Fung, Andriana Zeevi, and Rene Duruesnoy; Department of Pathology, University of Pittsburgh, Pittsburgh, PA

1986 ◽  
Vol 17 (2) ◽  
pp. 195-196
Keyword(s):  
T Cells ◽  
Endothelial Cells ◽  
University Of Pittsburgh ◽  
Alloreactive T Cells

scholarly journals Human Effector Memory CD4+ T Cells Directly Recognize Allogeneic Endothelial Cells In Vitro and In Vivo

2007 ◽  
Vol 179 (7) ◽  
pp. 4397-4404 ◽  
Author(s):  
Stephen L. Shiao ◽  
Nancy C. Kirkiles-Smith ◽  
Benjamin R. Shepherd ◽  
Jennifer M. McNiff ◽  
Edward J. Carr ◽  
...  
Keyword(s):  
T Cells ◽  
Endothelial Cells ◽  
Cd4 T Cells ◽  
Effector Memory ◽  
Memory Cd4 T Cells

ALLOANTIGEN-SPECFIC CD8+ T CELLS STIMULATE ENDOTHELIAL CELLS TO PRODUCE THE T CELL CHEMOATTRACTANTS IP-10 AND MIG.

2000 ◽  
Vol 69 (Supplement) ◽  
pp. S378
Author(s):  
Shoji Koga ◽  
Hirohito Kobayashi ◽  
Andrew C. Novick ◽  
Hiroshi Toma ◽  
Robert L. Fairchild
Keyword(s):  
T Cells ◽  
Endothelial Cells ◽  
T Cell ◽  
Cd8 T Cells

scholarly journals Regulatory T Cells Protect Fine Particulate Matter-Induced Inflammatory Responses in Human Umbilical Vein Endothelial Cells

2014 ◽  
Vol 2014 ◽  
pp. 1-14 ◽  
Author(s):  
Wen-cai Zhang ◽  
Yan-ge Wang ◽  
Zheng-feng Zhu ◽  
Fang-qin Wu ◽  
Yu-dong Peng ◽  
...  
Keyword(s):  
T Cells ◽  
Endothelial Cells ◽  
Particulate Matter ◽  
Inflammatory Cytokines ◽  
Fine Particles ◽  
Inflammatory Responses ◽  
Umbilical Vein ◽  
Fine Particulate Matter ◽  
Fine Particulate ◽  
Umbilical Vein Endothelial Cells

Objective. To investigate the role of CD4+CD25+T cells (Tregs) in protecting fine particulate matter (PM-) induced inflammatory responses, and its potential mechanisms.Methods. Human umbilical vein endothelial cells (HUVECs) were treated with graded concentrations (2, 5, 10, 20, and 40 µg/cm2) of suspension of fine particles for 24h. For coculture experiment, HUVECs were incubated alone, with CD4+CD25−T cells (Teff), or with Tregs in the presence of anti-CD3 monoclonal antibodies for 48 hours, and then were stimulated with or without suspension of fine particles for 24 hours. The expression of adhesion molecules and inflammatory cytokines was examined.Results. Adhesion molecules, including vascular cell adhesion molecule-1 (VCAM-1) and intercellular adhesion molecule-1 (ICAM-1), and inflammatory cytokines, such as interleukin (IL-) 6 and IL-8, were increased in a concentration-dependent manner. Moreover, the adhesion of human acute monocytic leukemia cells (THP-1) to endothelial cells was increased and NF-κB activity was upregulated in HUVECs after treatment with fine particles. However, after Tregs treatment, fine particles-induced inflammatory responses and NF-κB activation were significantly alleviated. Transwell experiments showed that Treg-mediated suppression of HUVECs inflammatory responses impaired by fine particles required cell contact and soluble factors.Conclusions. Tregs could attenuate fine particles-induced inflammatory responses and NF-κB activation in HUVECs.

The Rac activator Tiam1 controls efficient T-cell trafficking and route of transendothelial migration

Blood ◽  
2009 ◽  
Vol 113 (24) ◽  
pp. 6138-6147 ◽  
Author(s):  
Audrey Gérard ◽  
Rob A. van der Kammen ◽  
Hans Janssen ◽  
Saskia I. Ellenbroek ◽  
John G. Collard
Keyword(s):  
T Cells ◽  
Endothelial Cells ◽  
T Cell ◽  
Transendothelial Migration ◽  
Contact Hypersensitivity ◽  
Cell Trafficking ◽  
T Cell Trafficking ◽  
Cell Arrest

Abstract Migration toward chemoattractants is a hallmark of T-cell trafficking and is essential to produce an efficient immune response. Here, we have analyzed the function of the Rac activator Tiam1 in the control of T-cell trafficking and transendothelial migration. We found that Tiam1 is required for chemokine- and S1P-induced Rac activation and subsequent cell migration. As a result, Tiam1-deficient T cells show reduced chemotaxis in vitro, and impaired homing, egress, and contact hypersensitivity in vivo. Analysis of the T-cell transendothelial migration cascade revealed that PKCζ/Tiam1/Rac signaling is dispensable for T-cell arrest but is essential for the stabilization of polarization and efficient crawling of T cells on endothelial cells. T cells that lack Tiam1 predominantly transmigrate through individual endothelial cells (transcellular migration) rather than at endothelial junctions (paracellular migration), suggesting that T cells are able to change their route of transendothelial migration according to their polarization status and crawling capacity.

scholarly journals Role of IFNγ in Allograft Tolerance Mediated by CD4+CD25+Regulatory T Cells by Induction of IDO in Endothelial Cells

2007 ◽  
Vol 7 (11) ◽  
pp. 2472-2482 ◽  
Author(s):  
P. Thebault ◽  
T. Condamine ◽  
M. Heslan ◽  
M. Hill ◽  
I. Bernard ◽  
...  
Keyword(s):  
T Cells ◽  
Endothelial Cells ◽  
Regulatory T Cells

scholarly journals Immune function of the blood-brain barrier: incomplete presentation of protein (auto-)antigens by rat brain microvascular endothelium in vitro.

1990 ◽  
Vol 110 (5) ◽  
pp. 1757-1766 ◽  
Author(s):  
W Risau ◽  
B Engelhardt ◽  
H Wekerle
Keyword(s):  
T Cells ◽  
Endothelial Cells ◽  
T Cell ◽  
T Lymphocytes ◽  
Rat Brain ◽  
Blood Brain Barrier ◽  
T Cell Activation ◽  
Cell Activation ◽  
Ifn Gamma

The endothelial blood-brain barrier (BBB) has a critical role in controlling lymphocyte traffic into the central nervous system (CNS), both in physiological immunosurveillance, and in its pathological aberrations. The intercellular signals that possibly could induce lymphocytes to cross the BBB include immunogenic presentation of protein (auto-)antigens by BBB endothelia to circulating T lymphocytes. This concept has raised much, though controversial, attention. We approached this problem by analyzing in vitro immunospecific interactions between clonal rat T lymphocyte lines with syngeneic, stringently purified endothelial monolayer cultures from adult brain micro-vessels. The rat brain endothelia (RBE) were established from rat brain capillaries using double collagenase digestion, density gradient fractionation and selective cytolysis of contaminating pericytes by anti-Thy 1.1 antibodies and complement. Incubation with interferon-gamma in most of the brain-derived endothelial cells induced Ia-antigens in the cytoplasm and on the cell surface in some of the cells. Before the treatment, the cells were completely Ia-negative. Pericytes were unresponsive to IFN-gamma treatment. When confronted with syngeneic T cell lines specific for protein (auto-)antigens (e.g., ovalbumin and myelin basic protein, MBP), RBE were completely unable to induce antigen-specific proliferation of syngeneic T lymphocytes irrespective of pretreatment with IFN-gamma and of cell density. RBE were inert towards the T cells, and did not suppress T cell activation induced by other "professional" antigen presenting cells (APC) such as thymus-derived dendritic cells or macrophages. IFN-gamma-treated RBE were, however, susceptible to immunospecific T cell killing. They were lysed by MBP-specific T cells in the presence of the specific antigen or Con A. Antigen dependent lysis was restricted by the appropriate (MHC) class II product. We conclude that the interaction of brain endothelial cells with encephalitogenic T lymphocytes may involve recognition of antigen in the molecular context of relevant MHC products, but that this interaction per se is insufficient to initiate the full T cell activation program.

Sign in / Sign up

Export Citation Format

Share Document