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Oral lesions in lupus erythematosus–cytokines profiles of inflammatory infiltrate
Author(s) -
Marques Elisa R. M. C.,
Lourenço Silvia Vanessa,
Lima Dirce M.,
Nico Marcello Menta S.
Publication year - 2010
Publication title -
journal of cutaneous pathology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.597
H-Index - 75
eISSN - 1600-0560
pISSN - 0303-6987
DOI - 10.1111/j.1600-0560.2009.01424.x
Subject(s) - pathology , medicine , lupus erythematosus , systemic lupus erythematosus , inflammation , immunology , disease , antibody
Background: Lupus erythematosus (LE) is a chronic inflammatory disease. Presence of type 1 cytokines in cutaneous discoid lesions suggests that they may be critical for induction, development and maintenance of these manifestations. Type 2 cytokines in combination with local interferon gamma (INF‐γ) are thought to be related to the physiopathology of cutaneous LE. Cytokines profiles are still unknown in oral LE lesions. Materials and Methods: Expression of Th1 and Th2 cytokines (including IL‐4, IL‐5, IL‐6, IL‐10, IL‐12, tumor necrosis factor alpha (TNF‐α) and INF‐ γ was investigated and compared in 29 biopsies of intra‐oral (sun‐protected) and labial lesions (sun‐exposed) of LE using immunohistochemistry. Results: Inflammatory infiltrate of LE lesions was strongly positive for IFN‐ γ (97%) and TNF‐α (90%), both Th1 type cytokines. Interleukin‐10, a Th2 cytokine was also strongly expressed. Other cytokines were only mildly positive. Cytokines patterns were similar in intra‐oral (sun‐covered) and labial (sun‐exposed) LE lesions. Conclusions: Oral LE lesions are associated with both type 1 and type 2 cytokines, characterized by stronger expression of INF‐ γ, TNF‐ α and IL‐10. These findings suggest that although ultraviolet (UV) light is involved in the induction of LE lesions, mechanisms of lesions formation may be similar in sun‐exposed as well as sun‐covered areas. Marques ERMC, Lourenço SV, Lima DM, Nico MMS. Oral lesions in lupus erythematosus–cytokines profiles of inflammatory infiltrate.