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Clinic and pathophysiology of photosensitivity in lupus erythematosus.

Abstract

Lupus erythematosus (LE) represents an autoimmune disease with great clinical variability in which photosensitivity is a common feature for all forms and subsets. The nature and characteristics of clinical photosensitivity in LE have been elucidated through standardized phototesting procedures. The development of skin lesions after UV-injury is typically delayed starting from a few days up to three weeks after the irradiation, and may persist for months. Therefore, patients may not be aware of the detrimental effects of sunlight for their disease. The most photosensitive subset of LE is LE tumidus, followed by subacute cutaneous LE. Phototesting has also been crucial for studying the pathophysiology of LE-photosensitivity. Abnormalities of generation and clearance of UV-triggered apoptotic cells in LE are an important source of autoantigens. Recent data demonstrate the linkage of innate with adoptive immune pathways in UV-induced autoimmune response. Plasmocytoid dendritic cells (PDC) and their secreted IFN-alpha play a central role in the LE-pathogenesis. The recruitment of relevant leukocyte subsets is dependant on certain chemokines, which have been characterized in recent studies. An amplification cycle has been postulated, in which UV induces apoptosis and necrosis resulting in the production and release of chemokines. Subsequently, effector memory T cells as well as PDCs are recruited and activated perpetuating an amplification process that leads to UV-induced cutaneous LE lesion.

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  • Authors+Show Affiliations

    ,

    Dept of Dermatology, Allergology and Environmental Medicine, HELIOS Klinikum Wuppertal, University of Witten-Herdecke, Germany. Percy.Lehmann@HELIOS-Kliniken.de

    Source

    Autoimmunity reviews 8:6 2009 May pg 456-61

    MeSH

    Antigen Presentation
    Apoptosis
    Autoantigens
    Autoimmunity
    Chemokines
    Dendritic Cells
    Humans
    Immunologic Memory
    Lupus Erythematosus, Cutaneous
    Lupus Erythematosus, Systemic
    Photosensitivity Disorders
    Radiation Injuries
    Skin
    Sunlight
    T-Lymphocytes

    Pub Type(s)

    Journal Article
    Review

    Language

    eng

    PubMed ID

    19167524

    Citation

    Lehmann, Percy, and Bernhard Homey. "Clinic and Pathophysiology of Photosensitivity in Lupus Erythematosus." Autoimmunity Reviews, vol. 8, no. 6, 2009, pp. 456-61.
    Lehmann P, Homey B. Clinic and pathophysiology of photosensitivity in lupus erythematosus. Autoimmun Rev. 2009;8(6):456-61.
    Lehmann, P., & Homey, B. (2009). Clinic and pathophysiology of photosensitivity in lupus erythematosus. Autoimmunity Reviews, 8(6), pp. 456-61. doi:10.1016/j.autrev.2008.12.012.
    Lehmann P, Homey B. Clinic and Pathophysiology of Photosensitivity in Lupus Erythematosus. Autoimmun Rev. 2009;8(6):456-61. PubMed PMID: 19167524.
    * Article titles in AMA citation format should be in sentence-case
    TY - JOUR T1 - Clinic and pathophysiology of photosensitivity in lupus erythematosus. AU - Lehmann,Percy, AU - Homey,Bernhard, Y1 - 2009/01/22/ PY - 2009/1/27/entrez PY - 2009/1/27/pubmed PY - 2009/7/18/medline SP - 456 EP - 61 JF - Autoimmunity reviews JO - Autoimmun Rev VL - 8 IS - 6 N2 - Lupus erythematosus (LE) represents an autoimmune disease with great clinical variability in which photosensitivity is a common feature for all forms and subsets. The nature and characteristics of clinical photosensitivity in LE have been elucidated through standardized phototesting procedures. The development of skin lesions after UV-injury is typically delayed starting from a few days up to three weeks after the irradiation, and may persist for months. Therefore, patients may not be aware of the detrimental effects of sunlight for their disease. The most photosensitive subset of LE is LE tumidus, followed by subacute cutaneous LE. Phototesting has also been crucial for studying the pathophysiology of LE-photosensitivity. Abnormalities of generation and clearance of UV-triggered apoptotic cells in LE are an important source of autoantigens. Recent data demonstrate the linkage of innate with adoptive immune pathways in UV-induced autoimmune response. Plasmocytoid dendritic cells (PDC) and their secreted IFN-alpha play a central role in the LE-pathogenesis. The recruitment of relevant leukocyte subsets is dependant on certain chemokines, which have been characterized in recent studies. An amplification cycle has been postulated, in which UV induces apoptosis and necrosis resulting in the production and release of chemokines. Subsequently, effector memory T cells as well as PDCs are recruited and activated perpetuating an amplification process that leads to UV-induced cutaneous LE lesion. SN - 1873-0183 UR - https://www.unboundmedicine.com/medline/citation/19167524/full_citation L2 - https://linkinghub.elsevier.com/retrieve/pii/S1568-9972(08)00259-0 DB - PRIME DP - Unbound Medicine ER -