BACKGROUND: Erythema multiforme (EM) and Stevens-Johnson syndrome (SJS)/toxic epidermal necrolysis (TEN) are determined by a dysregulation of cellular immunity. OBJECTIVES: To evaluate the effector role of cellular immunity and the involvement of the CD40/CD40 ligand (CD40L) system in the pathogenesis of EM and SJS/TEN. METHODS: Biopsy specimens from eight patients with EM and six with SJS/TEN were stained for immunohistochemical examination using the alkaline phosphatase/antialkaline phosphatase method. The monoclonal antibodies used included those to CD1a, CD4, CD8, CD40, CD40L, CD68, Fas, Fas ligand (FasL) and myeloperoxidase. RESULTS: The cellular infiltrate in both EM and SJS/TEN lesions was composed mainly of T lymphocytes and CD68+ macrophages. We also detected large amounts of neutrophils. Fas and FasL were very highly expressed in SJS and TEN, but weakly in EM. CD40 staining was strong in all tissue sections; there were numerous CD40L+ cells in SJS/TEN but much fewer in EM. CONCLUSIONS: Activated T lymphocytes and macrophages, but also neutrophils, are presumably the main triggers of mucocutaneous damage in the SJS/TEN disease spectrum. The Fas/FasL system is significantly expressed in SJS/TEN lesions, but not in EM, where this apoptotic pathway presumably does not play a pivotal role in the epidermal damage. We suggest that the CD40/CD40L system may represent an important pathway of induction of SJS/TEN lesions, while in EM it would contribute to the immunoinflammation only as a second-line mechanism.
BACKGROUND:Erythema multiforme (EM) and Stevens-Johnson syndrome (SJS)/toxic epidermal necrolysis (TEN) are determined by a dysregulation of cellular immunity. OBJECTIVES: To evaluate the effector role of cellular immunity and the involvement of the CD40/CD40 ligand (CD40L) system in the pathogenesis of EM and SJS/TEN. METHODS: Biopsy specimens from eight patients with EM and six with SJS/TEN were stained for immunohistochemical examination using the alkaline phosphatase/antialkaline phosphatase method. The monoclonal antibodies used included those to CD1a, CD4, CD8, CD40, CD40L, CD68, Fas, Fas ligand (FasL) and myeloperoxidase. RESULTS: The cellular infiltrate in both EM and SJS/TEN lesions was composed mainly of T lymphocytes and CD68+ macrophages. We also detected large amounts of neutrophils. Fas and FasL were very highly expressed in SJS and TEN, but weakly in EM. CD40 staining was strong in all tissue sections; there were numerous CD40L+ cells in SJS/TEN but much fewer in EM. CONCLUSIONS: Activated T lymphocytes and macrophages, but also neutrophils, are presumably the main triggers of mucocutaneous damage in the SJS/TEN disease spectrum. The Fas/FasL system is significantly expressed in SJS/TEN lesions, but not in EM, where this apoptotic pathway presumably does not play a pivotal role in the epidermal damage. We suggest that the CD40/CD40L system may represent an important pathway of induction of SJS/TEN lesions, while in EM it would contribute to the immunoinflammation only as a second-line mechanism.
Authors: Rosa Maria Corrales; Cintia Sade de Paiva; De-Quan Li; William Johnson Farley; Johanna Tukler Henriksson; Jan Per Gustav Bergmanson; Stephen Carl Pflugfelder Journal: Invest Ophthalmol Vis Sci Date: 2011-06-01 Impact factor: 4.799
Authors: Xiaobo Zhang; Wei Chen; Cintia S De Paiva; Rosa M Corrales; Eugene A Volpe; Andrew J McClellan; William J Farley; De-Quan Li; Stephen C Pflugfelder Journal: Invest Ophthalmol Vis Sci Date: 2011-08-09 Impact factor: 4.799
Authors: Krystyna Romańska-Gocka; Jacek Gocki; Waldemar Placek; Barbara Zegarska; Paweł Krause Journal: Arch Med Sci Date: 2010-03-09 Impact factor: 3.318
Authors: Flavia S A Pelegrino; Eugene A Volpe; Niral B Gandhi; De-Quan Li; Stephen C Pflugfelder; Cintia S de Paiva Journal: Arthritis Res Ther Date: 2012-11-01 Impact factor: 5.156