Endothelial cells: Heparin modulates the induction of functional antigen presentation by IFN-γ

1997 ◽  
Vol 25 (2) ◽  
pp. 195S-195S ◽  
Author(s):  
DAVID A RIX ◽  
MICHAEL S DOUGLAS ◽  
MARIA P LEON ◽  
SIMI ALI ◽  
DAVID TALBOT ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Antigen Presentation ◽  
Ifn Γ

CD40 amplifies Fas-mediated apoptosis: a mechanism contributing to emphysema

2012 ◽  
Vol 303 (2) ◽  
pp. L141-L151 ◽  
Author(s):  
Ayako Shigeta ◽  
Yuji Tada ◽  
Ji-Yang Wang ◽  
Shunsuke Ishizaki ◽  
Junichi Tsuyusaki ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Epithelial Cells ◽  
Pulmonary Emphysema ◽  
Alveolar Epithelial Cells ◽  
Alveolar Cells ◽  
Alveolar Epithelial ◽  
Cd40 Stimulation ◽  
Ifn Γ ◽  
Apoptosis And Inflammation

Excessive apoptosis and prolonged inflammation of alveolar cells are associated with the pathogenesis of pulmonary emphysema. We aimed to determine whether CD40 affects alveolar epithelial cells and endothelial cells, with regard to evoking apoptosis and inflammation. Mice were repeatedly treated with agonistic-anti CD40 antibody (Ab), with or without agonistic-anti Fas Ab, and evaluated for apoptosis and inflammation in lungs. Human pulmonary microvascular endothelial cells and alveolar epithelial cells were treated with agonistic anti-CD40 Ab and/or anti-Fas Ab to see their direct effect on apoptosis and secretion of proinflammatory molecules in vitro. Furthermore, plasma soluble CD40 ligand (sCD40L) level was evaluated in patients with chronic obstructive pulmonary disease (COPD). In mice, inhaling agonistic anti-CD40 Ab induced moderate alveolar enlargement. CD40 stimulation, in combination with anti-Fas Ab, induced significant emphysematous changes and increased alveolar cell apoptosis. CD40 stimulation also enhanced IFN-γ-mediated emphysematous changes, not via apoptosis induction, but via inflammation with lymphocyte accumulation. In vitro, Fas-mediated apoptosis was enhanced by CD40 stimulation and IFN-γ in endothelial cells and by CD40 stimulation in epithelial cells. CD40 stimulation induced secretion of CCR5 ligands in endothelial cells, enhanced with IFN-γ. Plasma sCD40L levels were significantly increased in patients with COPD, inversely correlating to the percentage of forced expiratory volume in 1 s and positively correlating to low attenuation area score by CT scan, regardless of smoking history. Collectively CD40 plays a contributing role in the development of pulmonary emphysema by sensitizing Fas-mediated apoptosis in alveolar cells and increasing the secretion of proinflammatory chemokines.

scholarly journals Gamma Interferon Mediates Experimental Cerebral Malaria by Signaling within Both the Hematopoietic and Nonhematopoietic Compartments

2017 ◽  
Vol 85 (11) ◽  
Author(s):  
Ana Villegas-Mendez ◽  
Patrick Strangward ◽  
Tovah N. Shaw ◽  
Ivana Rajkovic ◽  
Vinko Tosevski ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Cerebral Malaria ◽  
Myeloid Cell ◽  
Gamma Interferon ◽  
Cell Populations ◽  
Experimental Cerebral Malaria ◽  
Cerebral Pathology ◽  
Multiple Cell ◽  
Ifn Γ

ABSTRACT Experimental cerebral malaria (ECM) is a gamma interferon (IFN-γ)-dependent syndrome. However, whether IFN-γ promotes ECM through direct and synergistic targeting of multiple cell populations or by acting primarily on a specific responsive cell type is currently unknown. Here, using a panel of cell- and compartment-specific IFN-γ receptor 2 (IFN-γR2)-deficient mice, we show that IFN-γ causes ECM by signaling within both the hematopoietic and nonhematopoietic compartments. Mechanistically, hematopoietic and nonhematopoietic compartment-specific IFN-γR signaling exerts additive effects in orchestrating intracerebral inflammation, leading to the development of ECM. Surprisingly, mice with specific deletion of IFN-γR2 expression on myeloid cells, T cells, or neurons were completely susceptible to terminal ECM. Utilizing a reductionist in vitro system, we show that synergistic IFN-γ and tumor necrosis factor (TNF) stimulation promotes strong activation of brain blood vessel endothelial cells. Combined, our data show that within the hematopoietic compartment, IFN-γ causes ECM by acting redundantly or by targeting non-T cell or non-myeloid cell populations. Within the nonhematopoietic compartment, brain endothelial cells, but not neurons, may be the major target of IFN-γ leading to ECM development. Collectively, our data provide information on how IFN-γ mediates the development of cerebral pathology during malaria infection.

Salvianolic acid B suppresses IFN-γ-induced JAK/STAT1 activation in endothelial cells

2011 ◽  
Vol 128 (6) ◽  
pp. 560-564 ◽  
Author(s):  
Shih Chung Chen ◽  
Yun Lian Lin ◽  
Bin Huang ◽  
Danny Ling Wang ◽  
Jing Jy Cheng
Keyword(s):  
Endothelial Cells ◽  
Salvianolic Acid B ◽  
Salvianolic Acid ◽  
Ifn Γ

scholarly journals Effect of interleukin-15 on depressed splenic dendritic cell functions following trauma-hemorrhage

2009 ◽  
Vol 296 (1) ◽  
pp. C124-C130 ◽  
Author(s):  
Takashi Kawasaki ◽  
Mashkoor A. Choudhry ◽  
Martin G. Schwacha ◽  
Kirby I. Bland ◽  
Irshad H. Chaudry
Keyword(s):  
Dendritic Cell ◽  
Antigen Presentation ◽  
Ex Vivo ◽  
Sham Operation ◽  
Dc Functions ◽  
Midline Laparotomy ◽  
Shed Blood ◽  
Cell Functions ◽  
Splenic Dendritic Cell ◽  
Ifn Γ

Although trauma-hemorrhage (T-H) induces suppressed splenic dendritic cell (DC) maturation and antigen presentation capacity, it remains unclear whether IL-15 modulates splenic DC functions. The aim of this study therefore was to investigate the effect of IL-15 on splenic DC functions after T-H. Male C3H/HeN mice (6–8 wk old) were randomly assigned to T-H or sham operation. T-H was induced by midline laparotomy and ∼90 min of hemorrhagic shock (blood pressure 35 mmHg), followed by fluid resuscitation (4× the shed blood volume in the form of Ringer lactate). Two hours later, mice were killed, splenic DCs were isolated, and the effects of exogenous IL-15 on their costimulatory factors, major histocompatibility class II expression, ability to produce cytokines, and antigen presentation were measured. The results indicate that IL-15 production capacity of splenic DCs was reduced following T-H. Ex vivo exposure to IL-15 attenuated the suppressed production of TNF-α, IL-6, and IFN-γ from splenic DCs following T-H. In addition, expression of surface antigen studies demonstrate that exogenous IL-15 attenuated T-H-induced downregulation of the activation of DC. The suppressed splenic DC antigen presentation function following T-H was also attenuated by IL-15 treatment. Moreover, IL-15 enhanced IL-12-induced IFN-γ production and antigen presentation by splenic DCs. These data suggest that ex vivo treatment with IL-15 following T-H provides beneficial effects on splenic DCs. The depression in IL-15 production by splenic DCs could contribute to the host's enhanced susceptibility to infections following T-H.

scholarly journals TNF-α, IL-4, and IFN-γ Regulate Differential Expression of P- and E-Selectin Expression by Porcine Aortic Endothelial Cells

2000 ◽  
Vol 164 (6) ◽  
pp. 3309-3315 ◽  
Author(s):  
Claire J. Stocker ◽  
Katharine L. Sugars ◽  
Olivier A. Harari ◽  
R. Clive Landis ◽  
Bernard J. Morley ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Differential Expression ◽  
Aortic Endothelial Cells ◽  
Tnf Α ◽  
Ifn Γ ◽  
Porcine Aortic Endothelial Cells ◽  
Aortic Endothelial

scholarly journals Regulation of T helper cell responses during antigen presentation by norepinephrine-exposed endothelial cells

Immunology ◽  
2017 ◽  
Vol 154 (1) ◽  
pp. 104-121 ◽  
Author(s):  
Linghui Xu ◽  
Wanhong Ding ◽  
Lori L. Stohl ◽  
Xi K. Zhou ◽  
Shayan Azizi ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Antigen Presentation ◽  
T Helper Cell ◽  
Helper Cell ◽  
T Helper ◽  
Cell Responses
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