We are analyzing https://link.springer.com/chapter/10.1007/978-0-387-89520-8_5.

Title:
The Role of FasL and Fas in Health and Disease | SpringerLink
Description:
The FS7-associated cell surface antigen (Fas, also named CD95, APO-1 or TNFRSF6) attracted considerable interest in the field of apoptosis research since its discovery in 1989. The groups of Shin Yonehara and Peter Krammer were the first reporting extensive apoptotic...
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Keywords {🔍}

google, scholar, pubmed, cas, article, fas, cell, ligand, apoptosis, death, immunol, cancer, human, biol, cells, med, expression, receptor, signaling, activation, tumor, nat, protein, res, exp, mice, chem, mol, soluble, liver, immune, role, factor, gene, caspase, vivo, induces, system, fasmediated, clin, tcell, tnf, rev, inhibition, sci, mouse, immunity, therapeutic, antigen, int,

Topics {✒️}

pigment epithelium-derived factor macrophages enhances il-1r1-toll fasl-fas-related therapeutic tools lethal graft-versus-host disease graft-versus-host disease model nf-kappab-dependent gene expression death-inducing signaling complex fas-mediated t-cell killing cycloheximide-sensitive factor occurs cell-surface antigen-restricted activation month download article/chapter islet beta-cell failure fas ligand-expressing grafts acute leukemic t-cells tumor necrosis factor mitogen-activated protein kinases post-endocytic sorting machinery cytokine-activated hematopoietic cells suppresses light-mediated apoptosis leukemic b-lymphoid cells activated b-cell death anti-fas ligand mab hypoxic-ischemic brain injury nf-kappab nuclear translocation ligand-independent oligomerization domain tumor-infiltrating lymphocytes induced activated t-cell death biased fas-signaling pathway acute t-cell leukemia cd95 ligand—death factor als-linked sod1 mutations lipopolysacharide-induced myocardial dysfunction monoclonal antibody-induced apoptosis cd40l-induced prosurvival signaling activation-dependent transcriptional regulation target cell-restricted triggering c-jun nh long-term graft survival receptor-mediated apoptosis induction cell-killing monoclonal antibody glycogen synthase kinase-3 t-cell apoptosis detected matrix metalloproteinase-7-mediated cleavage glucocorticoid-induced monocyte apoptosis fadd-homologous ice/ced-3 supramolecular fasl-fas clusters mature t-cell activation induces fas-dependent apoptosis normal human t-lymphocytes t-cell-deficient mice

Questions {❓}

CD95 ligand—Death factor and costimulatory molecule?
Immune privilege or inflammation?

Schema {🗺️}

ScholarlyArticle:
      headline:The Role of FasL and Fas in Health and Disease
      pageEnd:93
      pageStart:64
      image:https://media.springernature.com/w153/springer-static/cover/book/978-0-387-89520-8.jpg
      genre:
         Biomedical and Life Sciences
         Biomedical and Life Sciences (R0)
      isPartOf:
         name:Therapeutic Targets of the TNF Superfamily
         isbn:
            978-0-387-89520-8
            978-0-387-89519-2
         type:Book
      publisher:
         name:Springer New York
         logo:
            url:https://www.springernature.com/app-sn/public/images/logo-springernature.png
            type:ImageObject
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      author:
            name:Martin Ehrenschwender
            affiliation:
                  name:University of Wuerzburg
                  address:
                     name:Department of Molecular Internal Medicine, Medical Clinic and Polyclinic II, University of Wuerzburg, Wuerzburg, Germany
                     type:PostalAddress
                  type:Organization
            type:Person
            name:Harald Wajant
            affiliation:
                  name:University of Wuerzburg
                  address:
                     name:Department of Molecular Internal Medicine, Medical Clinic and Polyclinic II, University of Wuerzburg, Wuerzburg, Germany
                     type:PostalAddress
                  type:Organization
            type:Person
      keywords:FasL Expression, Immune Privilege, Soluble FasL, Membrane FasL
      description:The FS7-associated cell surface antigen (Fas, also named CD95, APO-1 or TNFRSF6) attracted considerable interest in the field of apoptosis research since its discovery in 1989. The groups of Shin Yonehara and Peter Krammer were the first reporting extensive apoptotic cell death induction upon treating cells with Fas-specific monoclonal antibodies.1,2 Cloning of Fas3 and its ligand,4,5 FasL (also known as CD178, CD95L or TNFSF6), laid the cornerstone in establishing this receptor-ligand system as a central regulator of apoptosis in mammals. Therapeutic exploitation of FasL-Fas-mediated cytotoxicity was soon an ambitous goal and during the last decade numerous strategies have been developed for its realization. In this chapter, we will briefly introduce essential general aspects of the FasL-Fas system before reviewing its physiological and pathophysiological relevance. Finally, FasL-Fas-related therapeutic tools and concepts will be addressed.
      datePublished:2009
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Book:
      name:Therapeutic Targets of the TNF Superfamily
      isbn:
         978-0-387-89520-8
         978-0-387-89519-2
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      name:Springer New York
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      name:University of Wuerzburg
      address:
         name:Department of Molecular Internal Medicine, Medical Clinic and Polyclinic II, University of Wuerzburg, Wuerzburg, Germany
         type:PostalAddress
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      address:
         name:Department of Molecular Internal Medicine, Medical Clinic and Polyclinic II, University of Wuerzburg, Wuerzburg, Germany
         type:PostalAddress
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            address:
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               type:PostalAddress
            type:Organization
      name:Harald Wajant
      affiliation:
            name:University of Wuerzburg
            address:
               name:Department of Molecular Internal Medicine, Medical Clinic and Polyclinic II, University of Wuerzburg, Wuerzburg, Germany
               type:PostalAddress
            type:Organization
PostalAddress:
      name:Department of Molecular Internal Medicine, Medical Clinic and Polyclinic II, University of Wuerzburg, Wuerzburg, Germany
      name:Department of Molecular Internal Medicine, Medical Clinic and Polyclinic II, University of Wuerzburg, Wuerzburg, Germany
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