title: Ultraviolet radiation can either suppress or induce expression of intercellular adhesion molecule 1 (ICAM-1) on the surface of cultured human keratinocytes.
abstract: 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 (100 mJ/cm2 of UVB) 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 (10 to 100 mJ/cm2), CD54 expression is significantly induced (p less than 0.01 to p less than 0.001) 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.
authors.affiliation: Department of Dermatology, University of Colorado Health Sciences Center, Denver.
authors.forename: D A
authors.initials: DA
authors.lastname: Norris
authors.forename: M B
authors.initials: MB
authors.lastname: Lyons
authors.forename: M H
authors.initials: MH
authors.lastname: Middleton
authors.forename: J J
authors.initials: JJ
authors.lastname: Yohn
authors.forename: M
authors.initials: M
authors.lastname: Kashihara-Sawami
mesh_terms: D015815:Cell Adhesion Molecules / Q000032:analysis / Q000096:biosynthesis*; D002462:Cell Membrane / Q000528:radiation effects; D002478:Cells, Cultured; D004307:Dose-Response Relationship, Radiation; D005434:Flow Cytometry; D005455:Fluorescent Antibody Technique; D006801:Humans; D066298:In Vitro Techniques; D007231:Infant, Newborn; D018799:Intercellular Adhesion Molecule-1; D015603:Keratinocytes / Q000378:metabolism / Q000528:radiation effects*; D007700:Kinetics; D011991:Receptors, Virus / Q000096:biosynthesis; D012867:Skin; D014466:Ultraviolet Rays
chemical_list: D015815:Cell Adhesion Molecules; D011991:Receptors, Virus; D018799:Intercellular Adhesion Molecule-1