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How to Assess Your Risk Using CHD Scoring Tests
Published in Mark C Houston, The Truth About Heart Disease, 2023
Biomarkers:MCP-3: immune cell direction and activity.sFas: prevents apoptosis (cell death).Fas ligand: initiates cell recycling and death.Eotaxin: activates immune cells in areas of injury.CTACK: helps to clean up damaged cells.IL-16: recruits and activates immune cells and indicates inflammation.HGF: stimulates tissue repair.
The maternal immune system during pregnancy
Published in Hung N. Winn, Frank A. Chervenak, Roberto Romero, Clinical Maternal-Fetal Medicine Online, 2021
In addition to the nonclassical MHC molecules, the tropho-blast expresses other antigens that may counter maternal immunosurveillance. The Fas ligand (FasL) binds to Fas expressed on target cells and results in the initiation of the target cell apoptosis pathway. Trophoblast constitutively expresses the FasL, while decidual NK cells express Fas. IFNg and TNF promote Fas expression and sensitivity, whereas IL-6 and IL-10 increase the resistance of trophoblast cells to Fas-mediated apoptosis (191).
Cytokines, Apoptosis, and Immune Therapy in HIV Infection
Published in Thomas F. Kresina, Immune Modulating Agents, 2020
Jerôme Estaquier, Jean-Claude Ameisen
Fas antibody-mediated and soluble Fas ligand-mediated apoptosis of CD4 and CD8 T cells from HIV-infected individuals may be prevented by pretreatment with the Ac-YVAD-CMK peptide, an irreversible competitive inhibitor of the ICE cysteine protease family [108]. Additional experiments using reversible aldehyde competitive inhibitors of cysteine protease specific to ICE (Ac-YVAD-CHO) and CPP32 (Ac-DEVD-CHO) have shown that Fas-mediated death signaling in T cells from HIV-infected individuals may involve the preferential activation of ICE in the CD4 T cells and of CPP32 in the CD8 T cells. Moreover, TCR-induced apoptosis of CD4 T cells is prevented by the competitive irreversible inhibitor of ICE (Ac-YVADCMK). This indicates that TCR-induced apoptosis of CD4 T cells from HIV-infected individuals involves the ICE protease cascade through Fas/FasL interaction, whereas pretreatment of CD8 T cells had no significant preventive effect on TCR-induced apoptosis. Although further work will be needed to confirm the precise nature of the proteases involved, our findings strongly suggest different pathways of programmed cell death and protease activations in CD4 and CD8 T cells from HIV-infected individuals.
Blood soluble Fas concentrations and ischemic stroke patient mortality
Published in Expert Review of Molecular Diagnostics, 2022
Leonardo Lorente, María M. Martín, Antonia Pérez-Cejas, Carmen Ferrer-Moure, Luis Ramos-Gómez, Jordi Solé-Violán, Juan J. Cáceres, Alejandro Jiménez, Agustín F. González-Rivero
One study had previously reported higher Fas expression in lymphocytes in ischemic stroke patients compared to healthy subjects and a positive correlation between Fas expression and stroke severity [11]. In another study of autopsies of fatal ischemic stroke and subjects who died due to other causes higher Fas expression was found in the brains of patients with ischemic stroke than in control subjects and in the homolateral hemisphere than in the contralateral hemisphere [12]. In another study, higher blood concentrations of sFas in ischemic stroke patients were found compared to control subjects with other neurologic disorders [13]. Activation of Fas by Fas ligand has been shown to be associated with activation of apoptosis and release of sFas [20]. However, to our knowledge, the novelties of our study were the existence of higher serum sFas levels in nonsurvivors than in survivors and the existence of an association between elevated blood sFas concentrations and mortality in patients with ischemic stroke.
Lessons from transmissible cancers for immunotherapy and transplant
Published in Immunological Medicine, 2022
Rafael Cardoso Maciel Costa Silva, Carolina Panis, Bruno Ricardo Barreto Pires
For a cell, tissue or organ to establish itself in a new organism, it must be nourished by the circulatory system's nutrients. This implies that the cells should possess the ability to adhere in an appropriate site for their metabolic needs or induce angiogenesis so that nutrients can diffuse and reach the ‘implanted’ cells. Similarly, cancer metastasis can only occur in appropriate sites, where the tumor cells can proliferate. Metastasis is also influenced by chemokines and chemoreceptors that direct cancerous cells to specific tissues [14]. After colonization, cells must avoid the immune response that will mediate the foreign tissue damage and rejection. Immune-privileged sites or a tolerogenic microenvironment (usually observed around cancers) facilitate cell implantation and proliferation through anti-inflammatory cytokines, like transforming growth factor β (TGF-β) and interleukin 10 (IL-10), that will ease immune responses [15,16]. Moreover, ligands that induce apoptosis, such as Fas ligand, contribute to this tolerogenic environment by inducing cell death of infiltrated immune cells. Apoptotic cells will further control inflammation after being recognized by scavenger receptors, leading to anti-inflammatory cytokines secretion. Nonetheless, the majority of transplants and cancers will occur in sites where there is no immune privilege.
A clinical and in-silico study exploring the association of CASP-3, NF-kB, miR-187, and miR-146 in pre-eclampsia
Published in Hypertension in Pregnancy, 2021
Charu Sharma, Purvi Purohit, Manoj Khokhar, Anupama Modi, Pratibha Singh, Shashank Shekhar, Shailja Sharma, Meenakshi Gothwal, Praveen Sharma
The current study, for the first time, reports the apoptosis gene CASP3, its regulatory transcription factor NF-κB and the regulatory MicroRNAs hsa-miR-146-5p and hsa-miR-187-5p in the blood samples and placental tissue of pre-eclamptic women. Recent studies have demonstrated apoptosis to have a significant role in the etiology and progression of PE. Apoptosis, defined as programmed cell death, is an important mechanism involved in maternal-fetal immune tolerance (19). In the extrinsic pathway mechanism, a cell expressing an FAS receptor on the surface binds to its FAS ligand, which activates a cascade of pro-apoptotic elements leading to cell death. The binding of FAS Ligand to the transmembrane receptor FAS recruits Pro-CASP-8. Subsequently, Pro-CASP-8 activates to CASP8 via the cleaving by procaspase and generating the active form of CASP3. The active CASP3 recruits other downstream effectors, eventually culmination in cell death (19). Placental development relies upon effective implantation and invasion of the maternal decidua (spiral arterioles) by the placental trophoblast. In normal pregnancy, trophoblast apoptosis increases with placental growth and advancing gestation. However, apoptosis is notably exaggerated in pregnancy complications like PE that is caused due to reduction of Maternal Blood flow in the intervillous space, hypoxic damage of the villous trophoblast leading to release of syncytiotrophoblast membrane fragments (20).