The Role of Graft Expressed Fas-Ligand on Allograft Rejection

2004 ◽  
Vol 106 (s50) ◽  
pp. 11P-11P
Author(s):  
MD Dooldeniya ◽  
F Morgan ◽  
PJ Dyson ◽  
AN Warrens
Keyword(s):  
Allograft Rejection ◽  
Fas Ligand

Role of Nitric Oxide and Superoxide in Acute Cardiac Allograft Rejection in Rats

2000 ◽  
Vol 225 (2) ◽  
pp. 151-159 ◽  
Author(s):  
Eiji Akizuki ◽  
Takaaki Akaike ◽  
Sinichirou Okamoto ◽  
Shigemoto Fujii ◽  
Yasuo Yamaguchi ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Allograft Rejection ◽  
Cardiac Allograft ◽  
Cardiac Allograft Rejection

scholarly journals Role of the IL-33/ST2 pathway in renal allograft rejection

2021 ◽  
pp. 112705
Author(s):  
Mi-Yeon Yu ◽  
Soie Kwon ◽  
Jong Joo Moon ◽  
Yong-Chul Kim ◽  
Eun Young Song ◽  
...  
Keyword(s):  
Allograft Rejection ◽  
Renal Allograft ◽  
Renal Allograft Rejection

scholarly journals sFasL—The Key to a Riddle: Immune Responses in Aging Lung and Disease

2021 ◽  
Vol 22 (4) ◽  
pp. 2177
Author(s):  
Shulamit B. Wallach-Dayan ◽  
Dmytro Petukhov ◽  
Ronit Ahdut-HaCohen ◽  
Mark Richter-Dayan ◽  
Raphael Breuer
Keyword(s):  
Cell Death ◽  
Lung Disease ◽  
Fas Ligand ◽  
Death Receptor ◽  
Mesenchymal Cells ◽  
Soluble Form ◽  
Cell Accumulation ◽  
Key Factor ◽  
Aged Subjects

By dint of the aging population and further deepened with the Covid-19 pandemic, lung disease has turned out to be a major cause of worldwide morbidity and mortality. The condition is exacerbated when the immune system further attacks the healthy, rather than the diseased, tissue within the lung. Governed by unremittingly proliferating mesenchymal cells and increased collagen deposition, if inflammation persists, as frequently occurs in aging lungs, the tissue develops tumors and/or turns into scars (fibrosis), with limited regenerative capacity and organ failure. Fas ligand (FasL, a ligand of the Fas cell death receptor) is a key factor in the regulation of these processes. FasL is primarily found in two forms: full length (membrane, or mFasL) and cleaved (soluble, or sFasL). We and others found that T-cells expressing the mFasL retain autoimmune surveillance that controls mesenchymal, as well as tumor cell accumulation following an inflammatory response. However, mesenchymal cells from fibrotic lungs, tumor cells, or cells from immune-privileged sites, resist FasL+ T-cell-induced cell death. The mechanisms involved are a counterattack of immune cells by FasL, by releasing a soluble form of FasL that competes with the membrane version, and inhibits their cell death, promoting cell survival. This review focuses on understanding the previously unrecognized role of FasL, and in particular its soluble form, sFasL, in the serum of aged subjects, and its association with the evolution of lung disease, paving the way to new methods of diagnosis and treatment.

scholarly journals Role of Fas ligand expression in promoting escape from immune rejection in a spontaneous tumor model

2001 ◽  
Vol 91 (4) ◽  
pp. 529-537 ◽  
Author(s):  
Daniel C�fai ◽  
Luc Favre ◽  
Elise Wattendorf ◽  
Andreas Marti ◽  
Rolf Jaggi ◽  
...  
Keyword(s):  
Fas Ligand ◽  
Tumor Model ◽  
Immune Rejection ◽  
Spontaneous Tumor ◽  
Ligand Expression

ROLE OF XANTHINE OXIDOREDUCTASE IN EXPERIMENTAL ACUTE RENAL-ALLOGRAFT REJECTION

2004 ◽  
Vol 77 (11) ◽  
pp. 1683-1692 ◽  
Author(s):  
Kai Sun ◽  
Eva Kiss ◽  
Jens Bedke ◽  
Tomislav Stojanovic ◽  
Yanhua Li ◽  
...  
Keyword(s):  
Allograft Rejection ◽  
Renal Allograft ◽  
Xanthine Oxidoreductase ◽  
Renal Allograft Rejection ◽  
Acute Renal Allograft Rejection

THE ROLE OF VASCULAR INJURY IN PULMONARY ALLOGRAFT REJECTION

1966 ◽  
Vol 4 (1) ◽  
pp. 66-78 ◽  
Author(s):  
MARTIN H. FLAX ◽  
BENJAMIN A. BARNES
Keyword(s):  
Vascular Injury ◽  
Allograft Rejection

scholarly journals Contribution of Fas ligand to cardiac allograft rejection

1996 ◽  
Vol 8 (9) ◽  
pp. 1347-1354 ◽  
Author(s):  
Kenichiro Seino ◽  
Nobuhiko Kayagaki ◽  
Hisashi Bashuda ◽  
Ko Okumura ◽  
Hideo Yagita ◽  
...  
Keyword(s):  
Allograft Rejection ◽  
Fas Ligand ◽  
Cardiac Allograft ◽  
Cardiac Allograft Rejection

Abstract 060: CCN1/a 6 β 1 Mediates Myocardial Injuries Induced by Work Overload or by Doxorubicin in Mice

2013 ◽  
Vol 113 (suppl_1) ◽  
Author(s):  
Pei-Ling I Hsu ◽  
Fan-E Mo
Keyword(s):  
Myocardial Injury ◽  
Fas Ligand ◽  
Cardiac Injury ◽  
Pressure Overload ◽  
Myocardial Damage ◽  
Matricellular Protein ◽  
Work Overload ◽  
Myocardial Injuries ◽  
Injury Models

Introduction: Matricellular protein CCN1 is expressed in myocardial infarction, pressure overload, and ischemia in mice, and in patients with a failing heart. Despite its well-documented angiogenic activities, CCN1 promotes fibroblast apoptosis in some contexts. The role of CCN1 in an injured heart was not clear. We assessed the hypothesis that CCN1 plays a detrimental role and mediates cardiac injury through its proapoptotic activities. Methods and Results: To test the role of CCN1 in cardiac injury, we employed two different myocardial injury models in mice, including a work-overload-induced injury created by isoproterenol treatment (ISO; 100 mg/kg/day; s.c. for 5 days; n= 6 for each group) and an injury induced by the cardiotoxicity of doxorubicin (DOX, single dose of 15 mg/kg; i.p. sacrificed after 14 days). Ccn1 expression was induced in the damaged myocardium in both injury models. A line of knock-in mice carrying an apoptosis-defective Ccn1 mutant allele, Ccn1-dm , which has disrupted integrin α 6 β 1 binding sites, were tested in the ISO- or DOX -induced cardiac injury. Myocardial damage was seen in tissues from wile-type (WT) hearts after receiving ISO. Ccn1 dm/dm (DM) mice possessed remarkable resistance against ISO or DOX treatments and exhibited no tissue damage or fibrosis compared to WT mice after H&E or Masson’s trichrome stainings. DM mice were resistant to both ISO- and DOX-induced cardiac cell apoptosis, indicating that CCN1 is critically mediating cardiomyocyte apoptotic death in cardiac injury. Moreover, we found that death factor Fas ligand (FasL) and its receptor Fas were upregulated in WT mice receiving ISO or DOX treatments by immunohistochemical staining, compared with the PBS-control. 8-OHdG-positive, a marker for oxidative stress, cardiomyocytes were increased by ISO or DOX treatments as well. In contrast, the expression of Fas/FasL, and the 8-OHdG-positive cardiomyocytes in the myocardium of DM mice were not changed by ISO or DOX. Conclusions: We identify CCN1 as a novel pathophysiological regulator of cardiomyocyte apoptosis in cardiac injury. Blocking apoptotic function of CCN1 effectively prevents myocardial injury in mice. CCN1 and its receptor α 6 β 1 represent promising future therapeutic targets in cardiac injury.

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