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Eosinophil Activation and In situ Interleukin‐5 Production by Mononuclear Cells in Skin Lesions of Patients with Drug Hypersensitivity
Author(s) -
Mikami Chikage,
Ochiai Kenichi,
Umemiya Keiko,
Matsumura Ryutarou,
Kagami Masaru,
Tomioka Hisao,
Sato Yuichi,
Tanabe Emiko
Publication year - 1999
Publication title -
the journal of dermatology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.9
H-Index - 65
eISSN - 1346-8138
pISSN - 0385-2407
DOI - 10.1111/j.1346-8138.1999.tb02064.x
Subject(s) - peripheral blood mononuclear cell , eosinophil , immunostaining , interleukin 5 , medicine , eosinophil cationic protein , pathology , interleukin , immunology , monoclonal antibody , in situ hybridization , inflammation , drug eruption , drug , immunohistochemistry , cytokine , antibody , chemistry , messenger rna , in vitro , pharmacology , biochemistry , asthma , gene
In order to determine the inflammatory mechanisms of skin lesions in patients with drug hypersentivity, we examined eosinophil activation and interleukin‐5 (IL‐5) production in infiltrating lymphocytes. First, we showed that the number of peripheral eosinophils and the level of serum IL‐5 at the eruption‐active stage were both significantly higher than those in healed skin eruptions. Histological and immunohistological examination revealed that CD4+ T cells and eosinophils significantly more densely infiltrated drug eruptions than control skin lesions. The infiltrating eosinophils were also shown to be activated by immunostaining using anti‐secreted formed eosinophilic cationic protein monoclonal antibody. The expression of mRNA for IL‐5 in the infiltrating mononuclear cells at drug eruptions was shown by in situ hybridization. These results suggest that infiltrating CD4+ T cells might regulate both peripheral and tissue eosinophils and facilitate allergic inflammation at drug eruptions by means of IL‐5 production.