Cellular adhesion antigen modulation in purpura pigmentosa chronica

Abstract

Background: Purpura pigmentosa chronica is an inflammatory skin disorder probably caused by an allergic reaction. Delayed-type hypersensitivity or immunocomplex vasculitis has been considered as a possible mechanism.

Objective: Detailed analysis of cell adhesion molecule (CAM) modulation may give further insights into the pathogenesis and underlying immune reaction of this disease.

Methods: By immunohistochemical techniques we investigated the in situ expression of integrins, selectins, and CAMs of the immunoglobulin superfamily.

Results: Infiltrating lymphocytes expressed LFA-1, LFA-2, VLA-4, and VLA-5, whereas some of the macrophages were also positive for p150/95 and MAC-1. VLA-1 was found on lymphocytes near the basement membrane of the epidermis. Compared with uninvolved or healthy skin endothelial cells showed upregulation of ICAM-1, VCAM-1, and, focally, E-selectin. Some fibroblasts were positive for ICAM-1. ICAM-1 was also upregulated on lesional keratinocytes that also expressed alpha 2, alpha 3, and alpha 6 integrin chains on basal and suprabasal epidermal layers.

Conclusion: Our findings demonstrate characteristic modifications in the expression of CAMs in purpura pigmentosa chronica and indicate the involvement of the epidermis in this disease. This modulation shows close parallels to those described for chronic delayed-type immune reactions of the skin.