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Updated: Jul 17, 2026
Granulocyte-dependent Autoantibody-induced Skin Blistering
Published on: October 12, 2012
Immunohistological analysis of immune cells in blistering skin lesions
Mahmoud R Hussein1, Fayed Mahammad Nagy Ali, Abd-Elhady M M Omar
1Department of Pathology, Faculty of Medicine, Assiut University Hospitals, Assiut University, Assiut, Egypt. mrh17@swissinfo.org
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< or =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.
