Tags

Type your tag names separated by a space and hit enter

Predominance of CD8 subset in id eruption of poison oak-induced dermatitis.
Australas J Dermatol. 1991; 32(2):93-100.AJ

Abstract

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.

Authors+Show Affiliations

Division of Dermatology, VA Medical Center, Sepulveda, California 91343.No affiliation info available

Pub Type(s)

Journal Article

Language

eng

PubMed ID

1838243

Citation

Heng, M C., and S G. Allen. "Predominance of CD8 Subset in Id Eruption of Poison Oak-induced Dermatitis." The Australasian Journal of Dermatology, vol. 32, no. 2, 1991, pp. 93-100.
Heng MC, Allen SG. Predominance of CD8 subset in id eruption of poison oak-induced dermatitis. Australas J Dermatol. 1991;32(2):93-100.
Heng, M. C., & Allen, S. G. (1991). Predominance of CD8 subset in id eruption of poison oak-induced dermatitis. The Australasian Journal of Dermatology, 32(2), 93-100.
Heng MC, Allen SG. Predominance of CD8 Subset in Id Eruption of Poison Oak-induced Dermatitis. Australas J Dermatol. 1991;32(2):93-100. PubMed PMID: 1838243.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Predominance of CD8 subset in id eruption of poison oak-induced dermatitis. AU - Heng,M C, AU - Allen,S G, PY - 1991/1/1/pubmed PY - 1991/1/1/medline PY - 1991/1/1/entrez SP - 93 EP - 100 JF - The Australasian journal of dermatology JO - Australas. J. Dermatol. VL - 32 IS - 2 N2 - 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. SN - 0004-8380 UR - https://www.unboundmedicine.com/medline/citation/1838243/Predominance_of_CD8_subset_in_id_eruption_of_poison_oak-induced_dermatitis L2 - https://onlinelibrary.wiley.com/resolve/openurl?genre=article&sid=nlm:pubmed&issn=0004-8380&date=1991&volume=32&issue=2&spage=93 DB - PRIME DP - Unbound Medicine ER -