These tools will no longer be maintained as of December 31, 2024. Archived website can be found here. PubMed4Hh GitHub repository can be found here. Contact NLM Customer Service if you have questions.


Pubmed for Handhelds

PUBMED FOR HANDHELDS

Search MEDLINE/PubMed

  • Title: Divergence of contact hypersensitivity in vivo compared with hapten-specific lymphocyte proliferation and interferon-gamma production in vitro following ultraviolet B irradiation: the possibility that UVB does not affect the sensitizing phase of contact hypersensitivity.
    Author: Suzuki K, Kanamori S, Takada K, Kawana S.
    Journal: Immunology; 2003 Apr; 108(4):570-8. PubMed ID: 12667220.
    Abstract:
    A hapten-specific lymphocyte proliferation assay, which measures the in vitro stimulation of DNA synthesis (as assessed by [3H]thymidine incorporation), was used to determine systemic immunization induced by an epicutaneously applied hapten in addition to the more commonly used method which measures ear (or footpad) swelling. 2,4-Dinitrofluorobenzene (DNFB) was painted on the shaved backs of C57BL/6 mice for two consecutive days after ultraviolet B (UVB) irradiation (at 1000 J/m2), and DNFB-sensitized lymph node cells (LNC) were obtained from the regional lymph nodes 4 days later. Although the ear swelling response (ESR) was suppressed by UVB radiation, as previously reported, analysis of LNC culture supernatants showed that the production of interferon-gamma, a Tc1-type cytokine, was not inhibited by the UVB irradiation. In addition, contact dermatitis was induced (at levels similar to those of non-irradiated mice) by painting DNFB on the abdomen as a secondary response. We then examined the effect of UVB exposure alone on the ESR by injecting a mast cell degranulator, compound 48/80, 7 days after irradiation. Both the ESR and the percentage of degranulated mast cells were significantly reduced in UVB-irradiated mice. These results demonstrate that UVB irradiation does not affect the sensitizing phase of contact hypersensitivity, but modulates the elicitation phase and reduces the ESR primarily by suppressing the degranulation of mast cells. Therefore, suppression of the ESR alone cannot always be considered as hapten-specific immunotolerance.
    [Abstract] [Full Text] [Related] [New Search]