Increased expression of human herpes virus 6 receptor CD134/OX40 in skin lesions of patients with drug‐induced hypersensitivity syndrome/drug reaction with eosinophilia and systemic symptoms. Issue 3 (19th September 2022)

• Record Type: Journal Article
• Authors: Lee, Eun Seon; Kiuchi, Yuji; Inomata, Naoko; Sueki, Hirohiko
• Other Names: Watanabe Daisuke guestEditor.
• Is Part Of: Journal of dermatology. Volume 50:Issue 3(2023)
• Page Start: 387
• Page End: 392
• Publication Date: 2022-09-19
• Subjects: CD134/OX40 -- drug reaction with eosinophilia and systemic symptoms -- drug‐induced hypersensitivity syndrome -- erythema multiforme -- human herpes virus‐6 receptor; Dermatology -- Periodicals; Dermatology -- Japan -- Periodicals; Skin -- Diseases -- Periodicals; 616.5005
• DOI: 10.1111/1346-8138.16575
• Languages: English
• ISSNs: 0385-2407

Abstract

Abstract: CD134/OX40, a member of the tumor necrosis factor receptor superfamily, is a cell‐specific receptor for human herpesvirus 6 (HHV‐6) variant B. Patients with drug‐induced hypersensitivity syndrome (DIHS)/drug reaction with eosinophilia and systemic symptoms (DRESS) present a significant increase in CD134 expression in peripheral blood CD4 + T cells. We aimed to investigate the frequency of CD134 + CD4 T cells infiltrating skin lesions in patients with DIHS/DRESS and its association with disease severity. We retrospectively included 21 patients with DIHS/DRESS and 11 patients with erythema multiforme (EM). By immunohistochemistry, the frequency of CD134 + CD4 T cells in DIHS was significantly higher than that in EM ( p = 0.0083). The DIHS/DRESS severity score was significantly correlated with the frequency of CD134 + CD4 T cells ( p = 0.0272); moreover, there was a significant difference between severe and mild/moderate cases. Double immunofluorescence staining revealed that numerous cells presented CD134/CD4 and CD134/Foxp3 overlap in patients with DIHS/DRESS. These data suggest increased susceptibility to HHV‐6 infection at localized skin sites. HHV‐6 may be involved in the mechanism underlying the progression and pathophysiology of DIHS/DRESS.