Document Detail

Type I interferon-associated cytotoxic inflammation in cutaneous lupus erythematosus.
MedLine Citation:
PMID:  18784932     Owner:  NLM     Status:  MEDLINE    
Inappropriate activation of innate immune mechanisms, in particular of the type I interferon (IFN) system, is regarded to play an important role in the pathogenesis of lupus erythematosus (LE). Type I IFN serum levels have been shown to correlate with the disease activity in systemic LE and additionally play a proinflammatory role in the development of LE skin lesions. Recent studies demonstrated a close morphological association between the expression pattern of IFN-inducible chemokines (MxA, CXCL10) and typical histological features of cutaneous LE. These and other studies suggest that a complex network of IFN-associated cytokines, chemokines and adhesion molecules orchestrates and promotes tissue injury observed in LE skin.
Joerg Wenzel; Sabine Zahn; Thomas Bieber; Thomas Tüting
Publication Detail:
Type:  Journal Article; Review     Date:  2008-09-11
Journal Detail:
Title:  Archives of dermatological research     Volume:  301     ISSN:  1432-069X     ISO Abbreviation:  Arch. Dermatol. Res.     Publication Date:  2009 Jan 
Date Detail:
Created Date:  2008-12-24     Completed Date:  2009-02-24     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  8000462     Medline TA:  Arch Dermatol Res     Country:  Germany    
Other Details:
Languages:  eng     Pagination:  83-6     Citation Subset:  IM    
Department of Dermatology, University of Bonn, Sigmund-Freud-Strasse 25, 53105 Bonn, Germany.
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MeSH Terms
Chemokines / immunology,  metabolism
Cytotoxicity, Immunologic
Homeostasis / immunology
Immunity, Innate
Interferon Type I / immunology*,  metabolism
Lupus Erythematosus, Cutaneous / immunology*,  metabolism,  physiopathology*
Lupus Erythematosus, Systemic / immunology,  metabolism,  physiopathology
T-Lymphocytes, Cytotoxic / immunology*,  metabolism
Toll-Like Receptors / immunology
Reg. No./Substance:
0/Chemokines; 0/Interferon Type I; 0/Toll-Like Receptors

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