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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 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 directmore » 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.« less

Authors:
; ; ; ;  [1]
  1. (Univ. of Colorado Health Sciences Center, Denver (USA))
Publication Date:
OSTI Identifier:
6521315
Resource Type:
Journal Article
Resource Relation:
Journal Name: Journal of Investigative Dermatology; (USA); Journal Volume: 95:2
Country of Publication:
United States
Language:
English
Subject:
63 RADIATION, THERMAL, AND OTHER ENVIRON. POLLUTANT EFFECTS ON LIVING ORGS. AND BIOL. MAT.; ANIMAL CELLS; BIOLOGICAL RADIATION EFFECTS; GROWTH FACTORS; BIOLOGICAL FUNCTIONS; LUPUS; RADIOINDUCTION; ADHESION; CELL CULTURES; CELL FLOW SYSTEMS; CELL MEMBRANES; DOSE-RESPONSE RELATIONSHIPS; FLUORESCENCE; IMMUNE REACTIONS; INHIBITION; INTERFERON; KERATIN; SKIN; ULTRAVIOLET RADIATION; VIRUSES; BACTERIAL DISEASES; BIOLOGICAL EFFECTS; BODY; CELL CONSTITUENTS; DISEASES; ELECTROMAGNETIC RADIATION; FUNCTIONS; IMMUNE SYSTEM DISEASES; INFECTIOUS DISEASES; LUMINESCENCE; LYMPHOKINES; MEMBRANES; MICROORGANISMS; MITOGENS; ORGANIC COMPOUNDS; ORGANS; PARASITES; PROTEINS; RADIATION EFFECTS; RADIATIONS; SCLEROPROTEINS; TUBERCULOSIS; 560120* - Radiation Effects on Biochemicals, Cells, & Tissue Culture

Citation Formats

Norris, D.A., Lyons, M.B., Middleton, M.H., Yohn, J.J., and Kashihara-Sawami, M. Ultraviolet radiation can either suppress or induce expression of intercellular adhesion molecule 1 (ICAM-1) on the surface of cultured human keratinocytes. United States: N. p., 1990. Web. doi:10.1111/1523-1747.ep12477877.
Norris, D.A., Lyons, M.B., Middleton, M.H., Yohn, J.J., & Kashihara-Sawami, M. Ultraviolet radiation can either suppress or induce expression of intercellular adhesion molecule 1 (ICAM-1) on the surface of cultured human keratinocytes. United States. doi:10.1111/1523-1747.ep12477877.
Norris, D.A., Lyons, M.B., Middleton, M.H., Yohn, J.J., and Kashihara-Sawami, M. 1990. "Ultraviolet radiation can either suppress or induce expression of intercellular adhesion molecule 1 (ICAM-1) on the surface of cultured human keratinocytes". United States. doi:10.1111/1523-1747.ep12477877.
@article{osti_6521315,
title = {Ultraviolet radiation can either suppress or induce expression of intercellular adhesion molecule 1 (ICAM-1) on the surface of cultured human keratinocytes},
author = {Norris, D.A. and Lyons, M.B. and Middleton, M.H. and Yohn, J.J. and Kashihara-Sawami, M.},
abstractNote = {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.},
doi = {10.1111/1523-1747.ep12477877},
journal = {Journal of Investigative Dermatology; (USA)},
number = ,
volume = 95:2,
place = {United States},
year = 1990,
month = 8
}