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Immunohistological analysis of immune cells in blistering skin lesions
  1. Mahmoud R Hussein,
  2. Fayed Mahammad Nagy Ali,
  3. Abd-Elhady M M Omar
  1. Department of Pathology, Faculty of Medicine, Assiut University Hospitals, Assiut University, Assiut, Egypt
  1. Correspondence to:
    Dr M R Hussein
    Department of Pathology, Faculty of Medicine, Assiut University Hospitals, Assiut, Egypt; mrh17{at}swissinfo.org

Abstract

Background: Bullous skin lesions are characterised by the presence of intraepidermal or subepidermal bullae. Although inflammatory cell infiltrate is a constant feature in these lesions, their immunophenotypic characterisation is still incomplete.

Aim: To determine whether the development of bullous skin diseases is associated with changes in the inflammatory cell infiltrate.

Materials and methods: 34 cases representing lesions with both intraepidermal and subepidermal bullae were examined using immunoperoxidase staining methods and antibodies targeting antigens for histiocytes (CD68), B cells (CD20+), T cells (CD3+), T cells with cytotoxic potential (T cell intracellular associated antigen, TIA1+) and activity (granzyme B, GRB+). The adjacent normal skin (lesions) and an additional five cases of normal skin were also examined (controls).

Results: The transition from normal skin to lesional skin (lesions with intraepidermal and subepidermal bullae) was associated with a significant increase (p⩽0.05) in the density of total inflammatory cell infiltrate, CD68+ cells, CD3+ T lymphocytes, CD20+ B lymphocytes, TIA1+-resting cytotoxic T cells and GRB+ T cells with cytotoxic activity.

Conclusions: The increase in inflammatory cell infiltrate during the transition from normal to lesional skin may reflect the presence of an increased antigenicity of the lesional cells or a response to some basement membrane components. CD68+ and CD3+ cells, especially the resting cytotoxic ones, achieved numerical dominance in these lesions. Cell-mediated immunity seems to have critical role in the development of these lesions.

  • CTL, cytotoxic T lymphocyte
  • GRB, granzyme B
  • TIA, T cell intracellular-associated antigen

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Footnotes

  • Competing interests: None declared.

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