Identification of type I interferon‐associated inflammation in the pathogenesis of cutaneous lupus erythematosus opens up options for novel therapeutic approaches
Identifieur interne : 001B42 ( Main/Exploration ); précédent : 001B41; suivant : 001B43Identification of type I interferon‐associated inflammation in the pathogenesis of cutaneous lupus erythematosus opens up options for novel therapeutic approaches
Auteurs : Joerg Wenzel [Allemagne] ; Thomas Tüting [Allemagne]Source :
- Experimental Dermatology [ 0906-6705 ] ; 2007-05.
English descriptors
- Teeft :
- Acad dermatol, Acta derm venereol, Adhesion, Adhesion molecules, Antinuclear antibodies, Antiviral, Apoptosis, Apoptotic, Apoptotic cells, Apoptotic keratinocytes, Arthritis rheum, Authors journal compilation, Autoantibody, Autoimmune, Autoimmune disorders, Blackwell munksgaard, Ccr4, Cdle, Chemokine, Chemokine receptor cxcr3, Chemokine receptors, Chemokines, Chloroquine, Clin, Clinical manifestations, Clinical observations, Cutaneous, Cutaneous lupus erythematosus, Cxcr3, Cytokine, Cytokine secretion, Cytotoxic, Cytotoxic lymphocytes, Dendritic, Dense perivascular, Dermatol, Dermatology, Disease activity, Eloranta, Epidermal, Erythematosus, Experimental dermatology, Ifns, Immune, Immune complexes, Immunol, Interferon, Large amounts, Lesion, Lesional, Lesional skin, Ligand, Lupus, Lupus erythematosus, Lupus erythematosus tumidus, Lymphocyte, Lymphocyte apoptosis, Lymphocyte recruitment, Methotrexate, Munksgaard, Natural cells, Ndings, Pathogenic, Pathogenic role, Pathway, Pdcs, Plasmacytoid, Plasmacytoid dendritic cells, Proc natl acad, Recent studies, Receptor, Rheum, Ronnblom, Skin lesions, Systemic, Systemic lupus erythematosus, Tlr9, Viral, Wenzel.
Abstract
Abstract: Cutaneous lupus erythematosus (CLE) is one of the most common dermatological autoimmune disorders worldwide. Recently, several studies provided evidence for a pathogenic role of type I interferons (IFNs) in this disease. Plasmacytoid dendritic cells are major type I IFN producers in CLE skin lesions. Type I IFNs are able to induce the expression of several proinflammatory chemokines, including CXCL9 and 10, and enhance the cytotoxic capacity of infiltrating cells. Additionally, adhesion molecules and chemokine receptors, such as intercellular adhesion molecule‐1, cutaneous lymphocyte antigen, E‐selectin, CCR4 and CXCR3, are involved in the recruitment of potentially autoreactive lymphocytes into the skin. Here, we review the role of type I IFNs, adhesion molecules and chemokine receptors in CLE and discuss options for novel therapeutic approaches.
Url:
DOI: 10.1111/j.1600-0625.2007.00556.x
Affiliations:
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munksgaard</term><term>Ccr4</term><term>Cdle</term><term>Chemokine</term><term>Chemokine receptor cxcr3</term><term>Chemokine receptors</term><term>Chemokines</term><term>Chloroquine</term><term>Clin</term><term>Clinical manifestations</term><term>Clinical observations</term><term>Cutaneous</term><term>Cutaneous lupus erythematosus</term><term>Cxcr3</term><term>Cytokine</term><term>Cytokine secretion</term><term>Cytotoxic</term><term>Cytotoxic lymphocytes</term><term>Dendritic</term><term>Dense perivascular</term><term>Dermatol</term><term>Dermatology</term><term>Disease activity</term><term>Eloranta</term><term>Epidermal</term><term>Erythematosus</term><term>Experimental dermatology</term><term>Ifns</term><term>Immune</term><term>Immune complexes</term><term>Immunol</term><term>Interferon</term><term>Large amounts</term><term>Lesion</term><term>Lesional</term><term>Lesional skin</term><term>Ligand</term><term>Lupus</term><term>Lupus erythematosus</term><term>Lupus erythematosus tumidus</term><term>Lymphocyte</term><term>Lymphocyte apoptosis</term><term>Lymphocyte recruitment</term><term>Methotrexate</term><term>Munksgaard</term><term>Natural cells</term><term>Ndings</term><term>Pathogenic</term><term>Pathogenic role</term><term>Pathway</term><term>Pdcs</term><term>Plasmacytoid</term><term>Plasmacytoid dendritic cells</term><term>Proc natl acad</term><term>Recent studies</term><term>Receptor</term><term>Rheum</term><term>Ronnblom</term><term>Skin lesions</term><term>Systemic</term><term>Systemic lupus erythematosus</term><term>Tlr9</term><term>Viral</term><term>Wenzel</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Abstract: Cutaneous lupus erythematosus (CLE) is one of the most common dermatological autoimmune disorders worldwide. Recently, several studies provided evidence for a pathogenic role of type I interferons (IFNs) in this disease. Plasmacytoid dendritic cells are major type I IFN producers in CLE skin lesions. Type I IFNs are able to induce the expression of several proinflammatory chemokines, including CXCL9 and 10, and enhance the cytotoxic capacity of infiltrating cells. Additionally, adhesion molecules and chemokine receptors, such as intercellular adhesion molecule‐1, cutaneous lymphocyte antigen, E‐selectin, CCR4 and CXCR3, are involved in the recruitment of potentially autoreactive lymphocytes into the skin. Here, we review the role of type I IFNs, adhesion molecules and chemokine receptors in CLE and discuss options for novel therapeutic approaches.</div></front></TEI><affiliations><list><country><li>Allemagne</li></country><region><li>District de Cologne</li><li>Rhénanie-du-Nord-Westphalie</li></region><settlement><li>Bonn</li></settlement></list><tree><country name="Allemagne"><region name="Rhénanie-du-Nord-Westphalie"><name sortKey="Wenzel, Joerg" sort="Wenzel, Joerg" uniqKey="Wenzel J" first="Joerg" last="Wenzel">Joerg Wenzel</name></region><name sortKey="Tuting, Thomas" sort="Tuting, Thomas" uniqKey="Tuting T" first="Thomas" last="Tüting">Thomas Tüting</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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