Epidermal keratinocytes of bullous pemphigoid express intercellular adhesion molecule-1 (ICAM-1)

T Karashima1, H Hachisuka, K Okubo

  • 1Department of Dermatology, Kurume University School of Medicine, Japan.

Insights

Intercellular adhesion molecule-1 (ICAM-1) and lymphocyte function-associated antigen-1 (LFA-1) are expressed in bullous pemphigoid skin lesions. This suggests a role for cellular immunity in the pathogenesis of bullous pemphigoid.

Area of Science:

  • Immunodermatology
  • Cellular immunology
  • Molecular biology

Background:

  • Intercellular adhesion molecule-1 (ICAM-1) binds lymphocyte function-associated antigen-1 (LFA-1), facilitating lymphocyte adhesion to endothelium.
  • Keratinocytes express ICAM-1 in inflammatory skin conditions.
  • The role of ICAM-1 and LFA-1 in bullous pemphigoid (BP) pathogenesis is not fully understood.

Purpose of the Study:

  • To investigate the expression patterns of ICAM-1 and LFA-1 in bullous pemphigoid (BP) lesions.
  • To compare ICAM-1 and LFA-1 expression in BP with pemphigus vulgaris (PV) and normal skin.
  • To explore the potential involvement of ICAM-1 and LFA-1 in the cellular immunity underlying BP.

Main Methods:

  • Indirect immunofluorescence staining was employed to detect ICAM-1 and LFA-1.
  • Skin biopsies from bullous pemphigoid (BP) patients, pemphigus vulgaris (PV) patients, and healthy controls were analyzed.
  • Immunohistochemical analysis focused on epidermal keratinocytes and cells within the dermal-تشinfiltrate.

Main Results:

  • ICAM-1 was expressed on keratinocytes in erythematous and bullous lesions of BP, but not in uninvolved skin, PV, or normal skin.
  • LFA-1 was detected on T cells located at the basement membrane zone in BP lesions.
  • HLA-DR-positive keratinocytes were observed in the basal layer of BP lesions.

Conclusions:

  • The expression of ICAM-1 on keratinocytes and LFA-1 on T cells in BP lesions suggests their involvement in the disease.
  • Cellular adhesion mediated by ICAM-1 and LFA-1 may contribute to the inflammatory process in bullous pemphigoid.
  • These findings highlight a potential role for cellular immunity in the pathogenesis of bullous pemphigoid.

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