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PREDOMINANCE OF CD8 SUBSET IN ID ERUPTION OF POISON OAK‐INDUCED DERMATITIS
Author(s) -
Heng Madalene C.Y.,
Allen Suni G.
Publication year - 1991
Publication title -
australasian journal of dermatology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.67
H-Index - 53
eISSN - 1440-0960
pISSN - 0004-8380
DOI - 10.1111/j.1440-0960.1991.tb00073.x
Subject(s) - immunology , antigen , cd8 , contact dermatitis , medicine , lymphokine , cytotoxic t cell , human leukocyte antigen , epidermis (zoology) , biology , in vitro , allergy , genetics , anatomy
S ummary 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 ofCD8+ 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.