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month download article/chapter early/rapid ros-independent release nephritic mrl-lpr/lpr mice cr-mediated oxidative metabolism cell death–related events friedrich-alexander universität erlangen-nürnberg histones h3-k27-me3 neutrophil-rich ocular surface kidney injury molecule-1 neutrophil extracellular trap neutrophil extracellular traps necrotic cell-derived chromatin oxidative burst-dependent netosis full article pdf acute abdominal inflammation cholesterol-induced death apoptotic human t-cells pediatric rheumatic diseases systemic lupus erythematosus cornelia erfurt-berge apolipoprotein e-deficient mice adaptive immune responses ps-dependent clearance heparin-induced thrombocytopenia cholesterol oxidation products privacy choices/manage cookies human neutrophil granulocytes sialic acid residues macrophage damage induced classical ros-dependent abc1 promotes engulfment mrl/lpr mice anti-inflammatory manner phosphatidylserine-ligand annexin a5 friedrich-alexander-universität related subjects article seminars german research foundation secondary necrosis generates prolonged cell death programmed cell death accidental cell death cell death pathways prototypic autoimmune disease autoimmune diseases systemic proinflammatory state increased positive selection chromatin-igg complexes chronic polyarthritis caused u1-70-kd antigen

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• Apoptosis, autophagic PCD, or others?
• Lood C, Allhorn M, Lood R, Gullstrand B, Olin AI, Ronnblom L, Truedsson L, Collin M, Bengtsson AA (2012) IgG glycan hydrolysis by endoglycosidase S diminishes the proinflammatory properties of immune complexes from patients with systemic lupus erythematosus: a possible new treatment?

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         headline:Towards a pro-resolving concept in systemic lupus erythematosus
         description:Systemic lupus erythematosus (SLE) is a prototypic autoimmune disease with prominent chronic inflammatory aspects. SLE most often affects women (9:1) in childbearing age. The multifactorial nature of the etiopathogenesis of SLE involves a deficient clearance of dead and dying cells. This is supported by the occurrence of autoantibodies directed against autoantigens modified in dying and dead cells (dsDNA, high mobility group box 1 protein, apoptosis-associated chromatin modifications, e.g., histones H3-K27-me3; H2A/H4 AcK8,12,16; and H2B-AcK12) that are deposited in various tissues, including skin, kidneys, joints, muscles, and brain. The subsequent hyperinflammatory response often leads to irreparable tissue damage and organ destruction. In healthy individuals, dead and dying cells are rapidly removed by macrophages in an anti-inflammatory manner, referred to as efferocytosis. In SLE, extensive and prolonged cell death (apoptosis, necrosis, neutrophil extracellular trap (NET) formation) leads to autoantigens leaking out of the not cleared cell debris. These neo-epitopes are subsequently presented to B cells by follicular dendritic cells in the germinal centers of secondary lymphoid tissues conditioning the break of self-tolerance. Activation of autoreactive B cells and subsequent production of autoantibodies facilitate the formation of immune complexes (ICs) fueling the inflammatory response and leading to further tissue damage. ICs may also be ingested by phagocytes, which then produce further pro-inflammatory cytokines. These processes establish a vicious circle that leads to sustained inflammation. This review highlights the cell death–related events in SLE, the protagonists involved in SLE pathogenesis, the resolution of inflammation in various tissues affected in SLE, and explores strategies for intervention to restore hemostasis in a hyperinflammatory state.
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      description:Systemic lupus erythematosus (SLE) is a prototypic autoimmune disease with prominent chronic inflammatory aspects. SLE most often affects women (9:1) in childbearing age. The multifactorial nature of the etiopathogenesis of SLE involves a deficient clearance of dead and dying cells. This is supported by the occurrence of autoantibodies directed against autoantigens modified in dying and dead cells (dsDNA, high mobility group box 1 protein, apoptosis-associated chromatin modifications, e.g., histones H3-K27-me3; H2A/H4 AcK8,12,16; and H2B-AcK12) that are deposited in various tissues, including skin, kidneys, joints, muscles, and brain. The subsequent hyperinflammatory response often leads to irreparable tissue damage and organ destruction. In healthy individuals, dead and dying cells are rapidly removed by macrophages in an anti-inflammatory manner, referred to as efferocytosis. In SLE, extensive and prolonged cell death (apoptosis, necrosis, neutrophil extracellular trap (NET) formation) leads to autoantigens leaking out of the not cleared cell debris. These neo-epitopes are subsequently presented to B cells by follicular dendritic cells in the germinal centers of secondary lymphoid tissues conditioning the break of self-tolerance. Activation of autoreactive B cells and subsequent production of autoantibodies facilitate the formation of immune complexes (ICs) fueling the inflammatory response and leading to further tissue damage. ICs may also be ingested by phagocytes, which then produce further pro-inflammatory cytokines. These processes establish a vicious circle that leads to sustained inflammation. This review highlights the cell death–related events in SLE, the protagonists involved in SLE pathogenesis, the resolution of inflammation in various tissues affected in SLE, and explores strategies for intervention to restore hemostasis in a hyperinflammatory state.
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      name:Cornelia Erfurt-Berge
      affiliation:
            name:Friedrich-Alexander-Universität (FAU) Erlangen-Nürnberg and Universitätsklinikum Erlangen
            address:
               name:Department of Dermatology, Friedrich-Alexander-Universität (FAU) Erlangen-Nürnberg and Universitätsklinikum Erlangen, Erlangen, Germany
               type:PostalAddress
            type:Organization
      name:Jürgen Rech
      affiliation:
            name:Friedrich-Alexander-Universität (FAU) Erlangen-Nürnberg, Universitätsklinikum Erlangen
            address:
               name:Department of Internal Medicine 3 – Rheumatology and Immunology, Friedrich-Alexander-Universität (FAU) Erlangen-Nürnberg, Universitätsklinikum Erlangen, Erlangen, Germany
               type:PostalAddress
            type:Organization
      name:Luis E. Muñoz
      affiliation:
            name:Friedrich-Alexander-Universität (FAU) Erlangen-Nürnberg, Universitätsklinikum Erlangen
            address:
               name:Department of Internal Medicine 3 – Rheumatology and Immunology, Friedrich-Alexander-Universität (FAU) Erlangen-Nürnberg, Universitätsklinikum Erlangen, Erlangen, Germany
               type:PostalAddress
            type:Organization
            name:Universitätsklinikum Erlangen
            address:
               name:Department of Internal Medicine 3, Universitätsklinikum Erlangen, Erlangen, Germany
               type:PostalAddress
            type:Organization
      email:[email protected]
      name:Martin Herrmann
      url:http://orcid.org/0000-0002-0258-2484
      affiliation:
            name:Friedrich-Alexander-Universität (FAU) Erlangen-Nürnberg, Universitätsklinikum Erlangen
            address:
               name:Department of Internal Medicine 3 – Rheumatology and Immunology, Friedrich-Alexander-Universität (FAU) Erlangen-Nürnberg, Universitätsklinikum Erlangen, Erlangen, Germany
               type:PostalAddress
            type:Organization
PostalAddress:
      name:Department of Internal Medicine 3 – Rheumatology and Immunology, Friedrich-Alexander-Universität (FAU) Erlangen-Nürnberg, Universitätsklinikum Erlangen, Erlangen, Germany
      name:Department of Internal Medicine 3 – Rheumatology and Immunology, Friedrich-Alexander-Universität (FAU) Erlangen-Nürnberg, Universitätsklinikum Erlangen, Erlangen, Germany
      name:Department of Internal Medicine 3 – Rheumatology and Immunology, Friedrich-Alexander-Universität (FAU) Erlangen-Nürnberg, Universitätsklinikum Erlangen, Erlangen, Germany
      name:Department of Internal Medicine 3 – Rheumatology and Immunology, Friedrich-Alexander-Universität (FAU) Erlangen-Nürnberg, Universitätsklinikum Erlangen, Erlangen, Germany
      name:Department of Internal Medicine 3 – Rheumatology and Immunology, Friedrich-Alexander-Universität (FAU) Erlangen-Nürnberg, Universitätsklinikum Erlangen, Erlangen, Germany
      name:Department of Rheumatology and Immunology, West China Hospital, Sichuan University, Chengdu, China
      name:Department of Internal Medicine 3 – Rheumatology and Immunology, Friedrich-Alexander-Universität (FAU) Erlangen-Nürnberg, Universitätsklinikum Erlangen, Erlangen, Germany
      name:Department of Dermatology, Friedrich-Alexander-Universität (FAU) Erlangen-Nürnberg and Universitätsklinikum Erlangen, Erlangen, Germany
      name:Department of Internal Medicine 3 – Rheumatology and Immunology, Friedrich-Alexander-Universität (FAU) Erlangen-Nürnberg, Universitätsklinikum Erlangen, Erlangen, Germany
      name:Department of Internal Medicine 3 – Rheumatology and Immunology, Friedrich-Alexander-Universität (FAU) Erlangen-Nürnberg, Universitätsklinikum Erlangen, Erlangen, Germany
      name:Department of Internal Medicine 3, Universitätsklinikum Erlangen, Erlangen, Germany
      name:Department of Internal Medicine 3 – Rheumatology and Immunology, Friedrich-Alexander-Universität (FAU) Erlangen-Nürnberg, Universitätsklinikum Erlangen, Erlangen, Germany
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