Immunophenotyping and viral studies in pityriasis lichenoides et varioliformis acuta lesions

Author:

Mishlab Salih12ORCID,Avitan‐Hersh Emily1,Zohar Yaniv2,Szwarcwort‐Cohen Moran3,Bergman Reuven12

Affiliation:

1. Department of Dermatology Rambam Health Care Campus and The Bruce Rappaport Faculty of Medicine Haifa Israel

2. Department of Pathology Rambam Health Care Campus and The Bruce Rappaport Faculty of Medicine Haifa Israel

3. Department of Microbiology Rambam Health Care Campus and The Bruce Rappaport Faculty of Medicine Haifa Israel

Abstract

AbstractBackgroundThe underlying pathogenesis of pityriasis lichenoides et varioliformis acuta (PLEVA) remains unclear, although immunologic injury and viral etiology have been suggested.ObjectiveTo evaluate and expand the immunophenotype of PLEVA and to search for possible viral pathogens.MethodsFormalin‐fixed, paraffin‐embedded specimens of 20 patients with PLEVA and 9 patients with common inflammatory dermatoses (ID) were studied for immunophenotyping and for human herpesvirus (HHV) 1 and 2, cytomegalovirus (CMV), HHV‐8, parvovirus B19, and Epstein–Barr virus (EBV) immunohistochemistry. The presence of HHV‐6, HHV‐7, and enteroviruses was assayed molecularly.ResultsThe numbers of CD8+ T cells and T‐cell intracellular antigen‐1 (TIA‐1)+ cells were statistically significantly higher in PLEVA compared to the ID group. Immunohistochemistry for human HHV‐1 and HHV‐2, CMV and HHV‐8, parvovirus B19, and in situ hybridization for EBV were all negative. There was molecular evidence for HHV‐7 in only one PLEVA case (5%). Molecular studies for HHV‐6 and enterovirus involvement were negative in all the PLEVA specimens.ConclusionsThe predominant T‐cell infiltrate in PLEVA is dominated by CD8+ cells, and by increased numbers of TIA1+ cells, which may indicate a cytotoxic T‐cell damage to the epidermis. Viral presence was not detected.

Publisher

Wiley

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