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Assessment of Oxidative Damage in the Primary Mouse Ocular Surface Cells/Stem Cells in Response to Ultraviolet-C (UV-C) Damage
Published on: February 15, 2020
UVA-induced immune suppression through an oxidative pathway
1Shiseido Research Center, Yokohama, Japan.
The Journal of Investigative Dermatology
|January 14, 1999
Summary
Ultraviolet A (UVA) irradiation suppresses skin immune responses by impairing antigen presentation and T cell proliferation. This immune suppression may be partly due to reactive oxygen species, as an antioxidant reversed the effects.
Area of Science:
- Immunology
- Dermatology
- Photobiology
Background:
- Ultraviolet B (UVB) is known to cause immune suppression.
- The effects of Ultraviolet A (UVA) on immune suppression are not well understood.
Purpose of the Study:
- To investigate the impact of UVA on immune responses in vitro and in vivo.
- To explore the role of reactive oxygen species in UVA-induced immune suppression.
Main Methods:
- Assessed UVA's effect on epidermal cell antigen-presenting function via T cell proliferation assays.
- Measured UVA's impact on Langerhans cell costimulatory molecules and ICAM-1 expression.
- Evaluated UVA's effect on contact hypersensitivity induction and lymph node cell proliferation ex vivo, with and without glutathione treatment.
Main Results:
- UVA dose-dependently suppressed epidermal cell antigen-presenting function and Langerhans cell costimulatory molecule expression.
- Glutathione significantly prevented UVA-induced suppression of antigen-presenting function and ICAM-1 expression.
- UVA irradiation suppressed lymph node cell proliferation in vivo, which was reversed by topical glutathione application.
Conclusions:
- UVA exposure induces immune suppression, affecting antigen presentation and T cell responses.
- Reactive oxygen species likely play a role in mediating UVA-induced immune suppression.
- Antioxidant intervention, like glutathione, can mitigate UVA-induced immunosuppression.
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