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Immunopathologic studies in pityriasis lichenoides.

A Giannetti1, G Girolomoni, C Pincelli

  • 1Department of Dermatology, University of Modena, Italy.

Archives of Dermatological Research
|January 1, 1988
PubMed
Summary
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Pityriasis lichenoides et varioliformis acuta and pityriasis lichenoides chronica share immune cell involvement, suggesting they are variants of a single skin disease. Cell-mediated immunity likely drives epidermal and vascular damage.

Area of Science:

  • Dermatology
  • Immunology
  • Pathology

Background:

  • Pityriasis lichenoides (PL) encompasses acute (PLEVA) and chronic (PLC) forms, differing in clinical presentation but potentially sharing underlying pathology.
  • Understanding the immune cell infiltrate in PL is crucial for elucidating its pathogenesis and potential therapeutic targets.

Purpose of the Study:

  • To investigate the immunophenotype of the inflammatory infiltrate in both PLEVA and PLC.
  • To compare immune cell populations between PLEVA and PLC to determine if they represent a spectrum of the same disease.
  • To explore the role of specific immune cells and antigen-presenting cells in the pathogenesis of skin lesions.

Main Methods:

  • Direct immunofluorescence and immunoperoxidase techniques were employed on skin biopsy specimens from patients with PLEVA and PLC.

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  • A panel of monoclonal antibodies was used to identify various immune cell populations, including T cells (CD4+, CD8+), macrophages, B cells, and CD1a+ cells.
  • Analysis focused on the distribution and predominance of immune cells within the epidermis and dermis.

    • Main Results:

    • The inflammatory infiltrate in both PLEVA and PLC consisted primarily of T cells and macrophages, with a small proportion of CD1a+ cells.
    • Epidermal CD8+ (cytotoxic/suppressor) T cells correlated with epidermal necrosis, while dermal CD4+ (helper/inducer) T cells were more numerous.
    • B cells and Leu7+ cells were infrequent. Endothelial cells expressing HLA-DR and HLA-DQ, and CD1a+ cells, were identified as potential antigen-presenting cells.

    Conclusions:

    • The similar immune cell profiles in PLEVA and PLC support the hypothesis that they are variants of a single disease process.
    • Cell-mediated immune mechanisms are implicated in the pathogenesis of epidermal and vascular damage observed in pityriasis lichenoides.
    • Antigen-presenting cells, including endothelial cells and CD1a+ cells, may play a key role in initiating and perpetuating the immune response.