Fluoroquinolone Eye Drop–Induced Cytotoxicity: Role of Preservative in P2X7 Cell Death Receptor Activation and Apoptosis

2006 ◽  
Vol 47 (7) ◽  
pp. 2812 ◽  
Author(s):  
Me´lody Dutot ◽  
Franc¸ois Pouzaud ◽  
Isabelle Larosche ◽  
Franc¸oise Brignole-Baudouin ◽  
Jean-Michel Warnet ◽  
...  
Keyword(s):  
Cell Death ◽  
Death Receptor ◽  
Receptor Activation ◽  
Cell Death Receptor

P2-209: Evaluation and modulation of toxic degenerative pathways induced by beta-amyloid on retinal cells: Role of P2X7 cell death receptor

2011 ◽  
Vol 7 ◽  
pp. S379-S380 ◽  
Author(s):  
Patrice Rat ◽  
Anais Wakx ◽  
Berengere De Moucheron ◽  
Melody Dutot ◽  
Olivier Laprevote
Keyword(s):  
Cell Death ◽  
Death Receptor ◽  
Beta Amyloid ◽  
Retinal Cells ◽  
Cell Death Receptor

scholarly journals The role of PD-1 – a programmed cell death receptor 1 – and its ligands in ovarian cancer immunotherapy

2016 ◽  
Vol 14 (2) ◽  
pp. 117-120 ◽  
Author(s):  
Anna Markowska ◽  
◽  
Stefan Sajdak ◽  
Jolanta Lubin ◽  
Janina Markowska ◽  
...  
Keyword(s):  
Ovarian Cancer ◽  
Cell Death ◽  
Programmed Cell Death ◽  
Cancer Immunotherapy ◽  
Death Receptor ◽  
Cell Death Receptor

Benefits and Side Effects of Different Vegetable Oil Vectors on Apoptosis, Oxidative Stress, and P2X7 Cell Death Receptor Activation

2007 ◽  
Vol 48 (11) ◽  
pp. 5000 ◽  
Author(s):  
Toihiri Said ◽  
Me´lody Dutot ◽  
Raymond Christon ◽  
Jean-Louis Beaudeux ◽  
Chantal Martin ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Cell Death ◽  
Side Effects ◽  
Vegetable Oil ◽  
Death Receptor ◽  
Receptor Activation ◽  
Cell Death Receptor

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.

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