This Article  • References  • Full text PDF  • Send to a friend  • Save in My Folder  • Save to citation manager  • Permissions  Citing Articles  • Citation map  • Citing articles on HighWire  • Contact me when this article is cited  Related Content  • Similar articles in this journal  Social Bookmarking   What's this?

Expression of Epidermal Keratinocyte Intercellular Adhesion Molecule-1 (ICAM-1)

Tetsuo Shiohara, MD, PhD; Brian J. Nickoloff, MD, PhD; Yoko Sagawa, MD; Toshihiko Gomi, MD; Masaji Nagashima, MD, PhD

Arch Dermatol. 1989;125(10):1371-1376.

Abstract
The pathogenic mechanism of preferential localization to certain skin sites of fixed drug eruption lesions has remained unknown. Skin biopsy specimens were obtained from four patients with fixed drug eruptions at various time points after final exposure to the causative drug and were studied immunohistologically using monoclonal antibodies to intercellular adhesion molecule-1 (ICAM-1), lymphocyte function-associated antigen-1, and HLA-DR. The expression of ICAM-1 by keratinocytes was confined exactly to the involved epidermis. In contrast, the expression of HLA-DR by keratinocytes was observed not only in the involved epidermis but also in the uninvolved epidermis, although to a lesser extent. In general, the intensity of expression of ICAM-1 by keratinocytes correlated well with the degree of epidermal invasion of lymphocytes but not with the degree of dermal lymphocytic infiltration. Interestingly, in fixed drug eruption lesions, basal keratinocytes still showed intense reactivity for ICAM-1 6 to 10 days after final exposure to the causative drug, at which time the expression of HLA-DR was already down-modulated. Such a strong dissociation between the expression of ICAM-1 and HLA-DR on lesional keratinocytes was never observed at any time in the normal skin of control patients challenged with dinitrochlorobenzene. These results suggest that localized misregulated expression of ICAM-1 by the keratinocytes may be one factor that explains the preferential site-specificity characteristic of fixed drug eruptions.

(Arch Dermatol. 1989;125:1371-1376)

Author Affiliations
From the Department of Dermatology, Kyorin University School of Medicine, Tokyo, Japan (Drs Shiohara, Sagawa, Gomi, and Nagashima); and the Departments of Pathology and Dermatology, University of Michigan Medical Center, Ann Arbor (Dr Nickoloff).

Footnotes
Accepted for publication March 28, 1989.

Reprint requests to Department of Dermatology, Kyorin University School of Medicine, 6-20-2 Shinkawa, Mitaka, Tokyo 181, Japan (Dr Shiohara).

CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    Twitter     What's this?

THIS ARTICLE HAS BEEN CITED BY OTHER ARTICLES

Effect of Arylhydroxylamine Metabolites of Sulfamethoxazole and Dapsone on Stress Signal Expression in Human Keratinocytes
Khan et al.
J. Pharmacol. Exp. Ther. 2007;323:771-777.
ABSTRACT | FULL TEXT  

Role of Delayed Cellular Hypersensitivity and Adhesion Molecules in Amoxicillin-Induced Morbilliform Rashes
Barbaud et al.
Arch Dermatol 1997;133:481-486.
ABSTRACT  

Multiply Recurrent Cellulitis-Reply
Manders and Heymann
Arch Dermatol 1996;132:1132-1132.
ABSTRACT  

Expression of Toxic Epidermal Necrolysis in Grafted Skin Is Donor-Site Dominant
Pion and Bystryn
Arch Dermatol 1993;129:1057-1058.
ABSTRACT  

Induction of the Intercellular Adhesion Molecule (ICAM-1) on Squamous Cell Carcinoma by Interferon Gamma
Scher et al.
Arch Otolaryngol Head Neck Surg 1993;119:432-438.
ABSTRACT  

Detection of the Interferon-gamma-Induced Protein 10 in Psoriasiform Dermatitis of Acquired Immunodeficiency Syndrome
Smoller et al.
Arch Dermatol 1990;126:1457-1461.
ABSTRACT