Ultraviolet radiation can either suppress or induce expression of intercellular adhesion molecule 1 (ICAM-1) on the surface of cultured human keratinocytes

Journal Article · Wed Aug 01 04:00:00 EDT 1990 · Journal of Investigative Dermatology; (USA)

DOI:https://doi.org/10.1111/1523-1747.ep12477877· OSTI ID:6521315

Norris, D A; Lyons, M B; Middleton, M H; Yohn, J J; Kashihara-Sawami, M ^[1]

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1. Univ. of Colorado Health Sciences Center, Denver (USA)

Interactions of the ligand/receptor pair LFA-1(CD11a/CD18) and ICAM-1(CD54) initiate and control the cell-cell interactions of leukocytes and interactions of leukocytes with parenchymal cells in all phases of the immune response. Induction of the intercellular adhesion molecule 1 (ICAM-1) on the surface of epidermal keratinocytes has been proposed as an important regulator of contact-dependent aspects of cutaneous inflammation. Ultraviolet radiation (UVR) also modifies cutaneous inflammation, producing both up- and down-regulation of contact hypersensitivity. We have found that UVR has a biphasic effect on the induction of keratinocyte CD54. Using immunofluorescence and FACS techniques to quantitate cell-surface CD54 staining, we have shown that UVR significantly (p less than 0.01) inhibits keratinocyte CD54 induction by gamma interferon 24 h after irradiation. However, at 48, 72, and 96 h after UVR, CD54 expression is significantly induced to levels even greater than are induced by gamma interferon (20 U/ml). In addition, at 48, 72, or 96 h following UVR (30-100 mJ/cm2), the gamma-interferon-induced CD54 expression on human keratinocytes is also strongly (p less than 0.05 to p less than 0.001) enhanced. In this cell-culture system, gamma interferon and TNF-alpha are both strong CD54 inducers and are synergistic, but GM-CSF, TFG-beta, and IL-1 have no direct CD54-inducing effects. Thus the effects of UVR on CD54 induction are biphasic, producing inhibition at 24 h and induction at 48, 72, and 96 h. This effect on CD54 may contribute to the biphasic effects of UVR on delayed hypersensitivity in vivo. The early inhibition of ICAM-1 by UVR may also contribute to the therapeutic effects of UVR. We also speculate that the late induction of ICAM-1 by UVR might be an important step in the induction of photosensitive diseases such as lupus erythematosus.

• OSTI ID: 6521315
• Journal Information: Journal of Investigative Dermatology; (USA), Journal Name: Journal of Investigative Dermatology; (USA) Vol. 95:2; ISSN 0022-202X; ISSN JIDEA
• Country of Publication: United States
• Language: English

Related Subjects

560120* -- Radiation Effects on Biochemicals
Cells
& Tissue Culture
63 RADIATION, THERMAL, AND OTHER ENVIRON. POLLUTANT EFFECTS ON LIVING ORGS. AND BIOL. MAT.
ADHESION
ANIMAL CELLS
BACTERIAL DISEASES
BIOLOGICAL EFFECTS
BIOLOGICAL FUNCTIONS
BIOLOGICAL RADIATION EFFECTS
BODY
CELL CONSTITUENTS
CELL CULTURES
CELL FLOW SYSTEMS
CELL MEMBRANES
DISEASES
DOSE-RESPONSE RELATIONSHIPS
ELECTROMAGNETIC RADIATION
FLUORESCENCE
FUNCTIONS
GROWTH FACTORS
IMMUNE REACTIONS
IMMUNE SYSTEM DISEASES
INFECTIOUS DISEASES
INHIBITION
INTERFERON
KERATIN
LUMINESCENCE
LUPUS
LYMPHOKINES
MEMBRANES
MICROORGANISMS
MITOGENS
ORGANIC COMPOUNDS
ORGANS
PARASITES
PROTEINS
RADIATION EFFECTS
RADIATIONS
RADIOINDUCTION
SCLEROPROTEINS
SKIN
TUBERCULOSIS
ULTRAVIOLET RADIATION
VIRUSES