Mechanisms of skin autoimmunity: Cellular and soluble immune components of the skin
Autoimmune diseases are driven by either T cells or antibodies reacting specifically to 1 or more self-antigens. Although a number of self-antigens associated with skin diseases have been identified, the causative antigen(s) remains unknown in the great majority of skin diseases suspected to be auto...
Ausführliche Beschreibung
Gespeichert in:
| Autor*in: |
Gudjonsson, Johann E. [verfasserIn] |
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| Format: |
E-Artikel |
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| Sprache: |
Englisch |
| Erschienen: |
2020transfer abstract |
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| Schlagwörter: |
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| Umfang: |
9 |
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| Übergeordnetes Werk: |
Enthalten in: Antidiabetic treatment in elderly patients with low performance status admitted to internal medicine ward - Papakitsou, I. ELSEVIER, 2022, official publication of the American Academy of Allergy, Asthma and Immunology, Amsterdam [u.a.] |
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| Übergeordnetes Werk: |
volume:146 ; year:2020 ; number:1 ; pages:8-16 ; extent:9 |
| Links: |
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| DOI / URN: |
10.1016/j.jaci.2020.05.009 |
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| 520 | |a Autoimmune diseases are driven by either T cells or antibodies reacting specifically to 1 or more self-antigens. Although a number of self-antigens associated with skin diseases have been identified, the causative antigen(s) remains unknown in the great majority of skin diseases suspected to be autoimmune driven. Model diseases such as pemphigus, dermatitis herpetiformis, and more recently psoriasis have added greatly to our understanding of skin autoimmunity. Depending on the dominant T- or B-cell phenotype, skin autoimmune diseases usually follow 1 of 6 immune response patterns: lichenoid, eczematous, bullous, psoriatic, fibrogenic, or granulomatous. Usually, skin autoimmunity develops as a consequence of several events—an altered microbiome, inherited dysfunctional immunity, antigens activating innate immunity, epigenetic modifications, sex predisposition, and impact of antigens either as neoantigen or through molecular mimicry. This review summarizes currently known antigens of skin autoimmune diseases and discusses mechanisms of skin autoimmunity. | ||
| 520 | |a Autoimmune diseases are driven by either T cells or antibodies reacting specifically to 1 or more self-antigens. Although a number of self-antigens associated with skin diseases have been identified, the causative antigen(s) remains unknown in the great majority of skin diseases suspected to be autoimmune driven. Model diseases such as pemphigus, dermatitis herpetiformis, and more recently psoriasis have added greatly to our understanding of skin autoimmunity. Depending on the dominant T- or B-cell phenotype, skin autoimmune diseases usually follow 1 of 6 immune response patterns: lichenoid, eczematous, bullous, psoriatic, fibrogenic, or granulomatous. Usually, skin autoimmunity develops as a consequence of several events—an altered microbiome, inherited dysfunctional immunity, antigens activating innate immunity, epigenetic modifications, sex predisposition, and impact of antigens either as neoantigen or through molecular mimicry. This review summarizes currently known antigens of skin autoimmune diseases and discusses mechanisms of skin autoimmunity. | ||
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10.1016/j.jaci.2020.05.009 doi /cbs_pica/cbs_olc/import_discovery/elsevier/einzuspielen/GBV00000000001302.pica (DE-627)ELV050792210 (ELSEVIER)S0091-6749(20)30686-2 DE-627 ger DE-627 rakwb eng 610 VZ 44.85 bkl Gudjonsson, Johann E. verfasserin aut Mechanisms of skin autoimmunity: Cellular and soluble immune components of the skin 2020transfer abstract 9 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Autoimmune diseases are driven by either T cells or antibodies reacting specifically to 1 or more self-antigens. Although a number of self-antigens associated with skin diseases have been identified, the causative antigen(s) remains unknown in the great majority of skin diseases suspected to be autoimmune driven. Model diseases such as pemphigus, dermatitis herpetiformis, and more recently psoriasis have added greatly to our understanding of skin autoimmunity. Depending on the dominant T- or B-cell phenotype, skin autoimmune diseases usually follow 1 of 6 immune response patterns: lichenoid, eczematous, bullous, psoriatic, fibrogenic, or granulomatous. Usually, skin autoimmunity develops as a consequence of several events—an altered microbiome, inherited dysfunctional immunity, antigens activating innate immunity, epigenetic modifications, sex predisposition, and impact of antigens either as neoantigen or through molecular mimicry. This review summarizes currently known antigens of skin autoimmune diseases and discusses mechanisms of skin autoimmunity. Autoimmune diseases are driven by either T cells or antibodies reacting specifically to 1 or more self-antigens. Although a number of self-antigens associated with skin diseases have been identified, the causative antigen(s) remains unknown in the great majority of skin diseases suspected to be autoimmune driven. Model diseases such as pemphigus, dermatitis herpetiformis, and more recently psoriasis have added greatly to our understanding of skin autoimmunity. Depending on the dominant T- or B-cell phenotype, skin autoimmune diseases usually follow 1 of 6 immune response patterns: lichenoid, eczematous, bullous, psoriatic, fibrogenic, or granulomatous. Usually, skin autoimmunity develops as a consequence of several events—an altered microbiome, inherited dysfunctional immunity, antigens activating innate immunity, epigenetic modifications, sex predisposition, and impact of antigens either as neoantigen or through molecular mimicry. This review summarizes currently known antigens of skin autoimmune diseases and discusses mechanisms of skin autoimmunity. Immune response pattern Elsevier B cell Elsevier autoimmunity Elsevier T cell Elsevier autoantigen Elsevier Kabashima, Kenji oth Eyerich, Kilian oth Enthalten in Elsevier Papakitsou, I. ELSEVIER Antidiabetic treatment in elderly patients with low performance status admitted to internal medicine ward 2022 official publication of the American Academy of Allergy, Asthma and Immunology Amsterdam [u.a.] (DE-627)ELV000021164 volume:146 year:2020 number:1 pages:8-16 extent:9 https://doi.org/10.1016/j.jaci.2020.05.009 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U SSG-OLC-PHA 44.85 Kardiologie Angiologie VZ AR 146 2020 1 8-16 9 |
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10.1016/j.jaci.2020.05.009 doi /cbs_pica/cbs_olc/import_discovery/elsevier/einzuspielen/GBV00000000001302.pica (DE-627)ELV050792210 (ELSEVIER)S0091-6749(20)30686-2 DE-627 ger DE-627 rakwb eng 610 VZ 44.85 bkl Gudjonsson, Johann E. verfasserin aut Mechanisms of skin autoimmunity: Cellular and soluble immune components of the skin 2020transfer abstract 9 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Autoimmune diseases are driven by either T cells or antibodies reacting specifically to 1 or more self-antigens. Although a number of self-antigens associated with skin diseases have been identified, the causative antigen(s) remains unknown in the great majority of skin diseases suspected to be autoimmune driven. Model diseases such as pemphigus, dermatitis herpetiformis, and more recently psoriasis have added greatly to our understanding of skin autoimmunity. Depending on the dominant T- or B-cell phenotype, skin autoimmune diseases usually follow 1 of 6 immune response patterns: lichenoid, eczematous, bullous, psoriatic, fibrogenic, or granulomatous. Usually, skin autoimmunity develops as a consequence of several events—an altered microbiome, inherited dysfunctional immunity, antigens activating innate immunity, epigenetic modifications, sex predisposition, and impact of antigens either as neoantigen or through molecular mimicry. This review summarizes currently known antigens of skin autoimmune diseases and discusses mechanisms of skin autoimmunity. Autoimmune diseases are driven by either T cells or antibodies reacting specifically to 1 or more self-antigens. Although a number of self-antigens associated with skin diseases have been identified, the causative antigen(s) remains unknown in the great majority of skin diseases suspected to be autoimmune driven. Model diseases such as pemphigus, dermatitis herpetiformis, and more recently psoriasis have added greatly to our understanding of skin autoimmunity. Depending on the dominant T- or B-cell phenotype, skin autoimmune diseases usually follow 1 of 6 immune response patterns: lichenoid, eczematous, bullous, psoriatic, fibrogenic, or granulomatous. Usually, skin autoimmunity develops as a consequence of several events—an altered microbiome, inherited dysfunctional immunity, antigens activating innate immunity, epigenetic modifications, sex predisposition, and impact of antigens either as neoantigen or through molecular mimicry. This review summarizes currently known antigens of skin autoimmune diseases and discusses mechanisms of skin autoimmunity. Immune response pattern Elsevier B cell Elsevier autoimmunity Elsevier T cell Elsevier autoantigen Elsevier Kabashima, Kenji oth Eyerich, Kilian oth Enthalten in Elsevier Papakitsou, I. ELSEVIER Antidiabetic treatment in elderly patients with low performance status admitted to internal medicine ward 2022 official publication of the American Academy of Allergy, Asthma and Immunology Amsterdam [u.a.] (DE-627)ELV000021164 volume:146 year:2020 number:1 pages:8-16 extent:9 https://doi.org/10.1016/j.jaci.2020.05.009 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U SSG-OLC-PHA 44.85 Kardiologie Angiologie VZ AR 146 2020 1 8-16 9 |
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10.1016/j.jaci.2020.05.009 doi /cbs_pica/cbs_olc/import_discovery/elsevier/einzuspielen/GBV00000000001302.pica (DE-627)ELV050792210 (ELSEVIER)S0091-6749(20)30686-2 DE-627 ger DE-627 rakwb eng 610 VZ 44.85 bkl Gudjonsson, Johann E. verfasserin aut Mechanisms of skin autoimmunity: Cellular and soluble immune components of the skin 2020transfer abstract 9 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Autoimmune diseases are driven by either T cells or antibodies reacting specifically to 1 or more self-antigens. Although a number of self-antigens associated with skin diseases have been identified, the causative antigen(s) remains unknown in the great majority of skin diseases suspected to be autoimmune driven. Model diseases such as pemphigus, dermatitis herpetiformis, and more recently psoriasis have added greatly to our understanding of skin autoimmunity. Depending on the dominant T- or B-cell phenotype, skin autoimmune diseases usually follow 1 of 6 immune response patterns: lichenoid, eczematous, bullous, psoriatic, fibrogenic, or granulomatous. Usually, skin autoimmunity develops as a consequence of several events—an altered microbiome, inherited dysfunctional immunity, antigens activating innate immunity, epigenetic modifications, sex predisposition, and impact of antigens either as neoantigen or through molecular mimicry. This review summarizes currently known antigens of skin autoimmune diseases and discusses mechanisms of skin autoimmunity. Autoimmune diseases are driven by either T cells or antibodies reacting specifically to 1 or more self-antigens. Although a number of self-antigens associated with skin diseases have been identified, the causative antigen(s) remains unknown in the great majority of skin diseases suspected to be autoimmune driven. Model diseases such as pemphigus, dermatitis herpetiformis, and more recently psoriasis have added greatly to our understanding of skin autoimmunity. Depending on the dominant T- or B-cell phenotype, skin autoimmune diseases usually follow 1 of 6 immune response patterns: lichenoid, eczematous, bullous, psoriatic, fibrogenic, or granulomatous. Usually, skin autoimmunity develops as a consequence of several events—an altered microbiome, inherited dysfunctional immunity, antigens activating innate immunity, epigenetic modifications, sex predisposition, and impact of antigens either as neoantigen or through molecular mimicry. This review summarizes currently known antigens of skin autoimmune diseases and discusses mechanisms of skin autoimmunity. Immune response pattern Elsevier B cell Elsevier autoimmunity Elsevier T cell Elsevier autoantigen Elsevier Kabashima, Kenji oth Eyerich, Kilian oth Enthalten in Elsevier Papakitsou, I. ELSEVIER Antidiabetic treatment in elderly patients with low performance status admitted to internal medicine ward 2022 official publication of the American Academy of Allergy, Asthma and Immunology Amsterdam [u.a.] (DE-627)ELV000021164 volume:146 year:2020 number:1 pages:8-16 extent:9 https://doi.org/10.1016/j.jaci.2020.05.009 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U SSG-OLC-PHA 44.85 Kardiologie Angiologie VZ AR 146 2020 1 8-16 9 |
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10.1016/j.jaci.2020.05.009 doi /cbs_pica/cbs_olc/import_discovery/elsevier/einzuspielen/GBV00000000001302.pica (DE-627)ELV050792210 (ELSEVIER)S0091-6749(20)30686-2 DE-627 ger DE-627 rakwb eng 610 VZ 44.85 bkl Gudjonsson, Johann E. verfasserin aut Mechanisms of skin autoimmunity: Cellular and soluble immune components of the skin 2020transfer abstract 9 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Autoimmune diseases are driven by either T cells or antibodies reacting specifically to 1 or more self-antigens. Although a number of self-antigens associated with skin diseases have been identified, the causative antigen(s) remains unknown in the great majority of skin diseases suspected to be autoimmune driven. Model diseases such as pemphigus, dermatitis herpetiformis, and more recently psoriasis have added greatly to our understanding of skin autoimmunity. Depending on the dominant T- or B-cell phenotype, skin autoimmune diseases usually follow 1 of 6 immune response patterns: lichenoid, eczematous, bullous, psoriatic, fibrogenic, or granulomatous. Usually, skin autoimmunity develops as a consequence of several events—an altered microbiome, inherited dysfunctional immunity, antigens activating innate immunity, epigenetic modifications, sex predisposition, and impact of antigens either as neoantigen or through molecular mimicry. This review summarizes currently known antigens of skin autoimmune diseases and discusses mechanisms of skin autoimmunity. Autoimmune diseases are driven by either T cells or antibodies reacting specifically to 1 or more self-antigens. Although a number of self-antigens associated with skin diseases have been identified, the causative antigen(s) remains unknown in the great majority of skin diseases suspected to be autoimmune driven. Model diseases such as pemphigus, dermatitis herpetiformis, and more recently psoriasis have added greatly to our understanding of skin autoimmunity. Depending on the dominant T- or B-cell phenotype, skin autoimmune diseases usually follow 1 of 6 immune response patterns: lichenoid, eczematous, bullous, psoriatic, fibrogenic, or granulomatous. Usually, skin autoimmunity develops as a consequence of several events—an altered microbiome, inherited dysfunctional immunity, antigens activating innate immunity, epigenetic modifications, sex predisposition, and impact of antigens either as neoantigen or through molecular mimicry. This review summarizes currently known antigens of skin autoimmune diseases and discusses mechanisms of skin autoimmunity. Immune response pattern Elsevier B cell Elsevier autoimmunity Elsevier T cell Elsevier autoantigen Elsevier Kabashima, Kenji oth Eyerich, Kilian oth Enthalten in Elsevier Papakitsou, I. ELSEVIER Antidiabetic treatment in elderly patients with low performance status admitted to internal medicine ward 2022 official publication of the American Academy of Allergy, Asthma and Immunology Amsterdam [u.a.] (DE-627)ELV000021164 volume:146 year:2020 number:1 pages:8-16 extent:9 https://doi.org/10.1016/j.jaci.2020.05.009 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U SSG-OLC-PHA 44.85 Kardiologie Angiologie VZ AR 146 2020 1 8-16 9 |
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10.1016/j.jaci.2020.05.009 doi /cbs_pica/cbs_olc/import_discovery/elsevier/einzuspielen/GBV00000000001302.pica (DE-627)ELV050792210 (ELSEVIER)S0091-6749(20)30686-2 DE-627 ger DE-627 rakwb eng 610 VZ 44.85 bkl Gudjonsson, Johann E. verfasserin aut Mechanisms of skin autoimmunity: Cellular and soluble immune components of the skin 2020transfer abstract 9 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Autoimmune diseases are driven by either T cells or antibodies reacting specifically to 1 or more self-antigens. Although a number of self-antigens associated with skin diseases have been identified, the causative antigen(s) remains unknown in the great majority of skin diseases suspected to be autoimmune driven. Model diseases such as pemphigus, dermatitis herpetiformis, and more recently psoriasis have added greatly to our understanding of skin autoimmunity. Depending on the dominant T- or B-cell phenotype, skin autoimmune diseases usually follow 1 of 6 immune response patterns: lichenoid, eczematous, bullous, psoriatic, fibrogenic, or granulomatous. Usually, skin autoimmunity develops as a consequence of several events—an altered microbiome, inherited dysfunctional immunity, antigens activating innate immunity, epigenetic modifications, sex predisposition, and impact of antigens either as neoantigen or through molecular mimicry. This review summarizes currently known antigens of skin autoimmune diseases and discusses mechanisms of skin autoimmunity. Autoimmune diseases are driven by either T cells or antibodies reacting specifically to 1 or more self-antigens. Although a number of self-antigens associated with skin diseases have been identified, the causative antigen(s) remains unknown in the great majority of skin diseases suspected to be autoimmune driven. Model diseases such as pemphigus, dermatitis herpetiformis, and more recently psoriasis have added greatly to our understanding of skin autoimmunity. Depending on the dominant T- or B-cell phenotype, skin autoimmune diseases usually follow 1 of 6 immune response patterns: lichenoid, eczematous, bullous, psoriatic, fibrogenic, or granulomatous. Usually, skin autoimmunity develops as a consequence of several events—an altered microbiome, inherited dysfunctional immunity, antigens activating innate immunity, epigenetic modifications, sex predisposition, and impact of antigens either as neoantigen or through molecular mimicry. This review summarizes currently known antigens of skin autoimmune diseases and discusses mechanisms of skin autoimmunity. Immune response pattern Elsevier B cell Elsevier autoimmunity Elsevier T cell Elsevier autoantigen Elsevier Kabashima, Kenji oth Eyerich, Kilian oth Enthalten in Elsevier Papakitsou, I. ELSEVIER Antidiabetic treatment in elderly patients with low performance status admitted to internal medicine ward 2022 official publication of the American Academy of Allergy, Asthma and Immunology Amsterdam [u.a.] (DE-627)ELV000021164 volume:146 year:2020 number:1 pages:8-16 extent:9 https://doi.org/10.1016/j.jaci.2020.05.009 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U SSG-OLC-PHA 44.85 Kardiologie Angiologie VZ AR 146 2020 1 8-16 9 |
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Enthalten in Antidiabetic treatment in elderly patients with low performance status admitted to internal medicine ward Amsterdam [u.a.] volume:146 year:2020 number:1 pages:8-16 extent:9 |
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mechanisms of skin autoimmunity: cellular and soluble immune components of the skin |
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Mechanisms of skin autoimmunity: Cellular and soluble immune components of the skin |
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Autoimmune diseases are driven by either T cells or antibodies reacting specifically to 1 or more self-antigens. Although a number of self-antigens associated with skin diseases have been identified, the causative antigen(s) remains unknown in the great majority of skin diseases suspected to be autoimmune driven. Model diseases such as pemphigus, dermatitis herpetiformis, and more recently psoriasis have added greatly to our understanding of skin autoimmunity. Depending on the dominant T- or B-cell phenotype, skin autoimmune diseases usually follow 1 of 6 immune response patterns: lichenoid, eczematous, bullous, psoriatic, fibrogenic, or granulomatous. Usually, skin autoimmunity develops as a consequence of several events—an altered microbiome, inherited dysfunctional immunity, antigens activating innate immunity, epigenetic modifications, sex predisposition, and impact of antigens either as neoantigen or through molecular mimicry. This review summarizes currently known antigens of skin autoimmune diseases and discusses mechanisms of skin autoimmunity. |
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Autoimmune diseases are driven by either T cells or antibodies reacting specifically to 1 or more self-antigens. Although a number of self-antigens associated with skin diseases have been identified, the causative antigen(s) remains unknown in the great majority of skin diseases suspected to be autoimmune driven. Model diseases such as pemphigus, dermatitis herpetiformis, and more recently psoriasis have added greatly to our understanding of skin autoimmunity. Depending on the dominant T- or B-cell phenotype, skin autoimmune diseases usually follow 1 of 6 immune response patterns: lichenoid, eczematous, bullous, psoriatic, fibrogenic, or granulomatous. Usually, skin autoimmunity develops as a consequence of several events—an altered microbiome, inherited dysfunctional immunity, antigens activating innate immunity, epigenetic modifications, sex predisposition, and impact of antigens either as neoantigen or through molecular mimicry. This review summarizes currently known antigens of skin autoimmune diseases and discusses mechanisms of skin autoimmunity. |
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Autoimmune diseases are driven by either T cells or antibodies reacting specifically to 1 or more self-antigens. Although a number of self-antigens associated with skin diseases have been identified, the causative antigen(s) remains unknown in the great majority of skin diseases suspected to be autoimmune driven. Model diseases such as pemphigus, dermatitis herpetiformis, and more recently psoriasis have added greatly to our understanding of skin autoimmunity. Depending on the dominant T- or B-cell phenotype, skin autoimmune diseases usually follow 1 of 6 immune response patterns: lichenoid, eczematous, bullous, psoriatic, fibrogenic, or granulomatous. Usually, skin autoimmunity develops as a consequence of several events—an altered microbiome, inherited dysfunctional immunity, antigens activating innate immunity, epigenetic modifications, sex predisposition, and impact of antigens either as neoantigen or through molecular mimicry. This review summarizes currently known antigens of skin autoimmune diseases and discusses mechanisms of skin autoimmunity. |
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