Predominance of CD8 subset in id eruption of poison oak-induced dermatitis.
The pathophysiology and immune mechanisms involved in the clinical syndrome of autoeczematization remain a mystery. In this study of nickel dermatitis without autoeczematization and poison oak dermatitis with autoeczematization, it was noted that the process of autoeczematization was associated with the presence of CD8+ lymphocytes within the epidermis and the expression of HLA-DR antigens on epidermal keratinocytes. It is surmised that since CD8+ clones are induced by poison oak antigen but not by nickel, the inability of nickel to induce CD8+ lymphocytes may explain why uncomplicated nickel dermatitis does not autoeczematize. Since the selective adherence of CD8+ lymphocytes to keratinocytes, probably via the expression of adhesion molecules such as ICAM-1, the generation of antigens on endothelial cells of high endothelial venules involved in lymphocyte trafficking, and the expression of HLA-DR antigens on epidermal keratinocytes are all due to the activity of interferon-8, it is deduced that this lymphokine may play a key role in id eruptions induced by contact allergens.
Heng
M C
MC
Division of Dermatology, VA Medical Center, Sepulveda, California 91343.
Allen
S G
SG
D016827:CD8 Antigens / Q000032:analysis*; D003877:Dermatitis, Contact / Q000276:immunology; D011040:Dermatitis, Toxicodendron / Q000276:immunology* / Q000473:pathology; D004485:Eczema / Q000276:immunology / Q000473:pathology; D006684:HLA-DR Antigens / Q000032:analysis; D006801:Humans; D016131:Lymphocyte Subsets / Q000276:immunology* / Q000473:pathology; D009532:Nickel / Q000009:adverse effects
D016827:CD8 Antigens; D006684:HLA-DR Antigens; D009532:Nickel