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Epidermal cell-contra-interleukin 1 inhibits human accessory cell function by specifically blocking interleukin 1
J Krutmann1, T Schwarz, R Kirnbauer
1Department of Dermatology II, University of Vienna, Austria.
Photochemistry and Photobiology
|October 1, 1990
Summary
Ultraviolet B (UVB) radiation suppresses immune responses by producing a factor that blocks Interleukin-1 (IL-1) activity. This UVB-inducible factor inhibits human accessory cell function, offering a novel immune modulation mechanism.
Area of Science:
- Immunology
- Dermatology
- Cell Biology
Background:
- Ultraviolet B (UVB) radiation can suppress cell-mediated immunity by affecting antigen-presenting cells.
- Human keratinocytes and carcinoma cells secrete a suppressor factor (hEC-contra-IL 1) upon UVB exposure, which inhibits Interleukin-1 (IL-1) activity.
Purpose of the Study:
- To investigate the capacity of the UVB-inducible cytokine, hEC-contra-IL 1, to modulate human accessory cell function.
- To elucidate the mechanism by which UVB radiation influences immune responses via accessory cells.
Main Methods:
- Human peripheral blood mononuclear cells were stimulated with anti-CD3 monoclonal antibody (OKT3).
- T-cell proliferation, measured by thymidine incorporation, served as an index for monocyte accessory cell activity.
- hEC-contra-IL 1 was purified using HPLC chromatography and its effects were assessed in the presence and absence of accessory cells.
Main Results:
- Purified hEC-contra-IL 1 partially inhibited OKT3-induced T-cell proliferation in a dose-dependent manner.
- hEC-contra-IL 1 did not inhibit T-cell blastogenesis when accessory cells were depleted, indicating accessory cell dependence.
- Recombinant human IL-1 (rhIL-1), but not rhIL-6, reconstituted the suppressed blastogenesis, and antibodies against IL-1 alpha/beta did not block the inhibitory effect of hEC-contra-IL 1.
Conclusions:
- hEC-contra-IL 1 suppresses human accessory cell function by specifically blocking IL-1 activity.
- This finding reveals a novel indirect mechanism through which UVB radiation modulates human accessory cell function.