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Related Experiment Video

Updated: May 20, 2026

Contact Hypersensitivity as a Murine Model of Allergic Contact Dermatitis

Contact Hypersensitivity as a Murine Model of Allergic Contact Dermatitis

Published on: September 26, 2022

Biological clock dysfunction exacerbates contact hypersensitivity in mice.

E Takita¹, S Yokota, Y Tahara

¹Department of Physiology and Pharmacology, School of Advanced Science and Engineering, Waseda University, Tokyo, Japan.

The British Journal of Dermatology

|July 28, 2012

Summary

Biological clock dysfunction exacerbates contact hypersensitivity (CHS) by promoting T-helper type 2 immune responses. Circadian rhythm disruption impacts corticosterone levels, highlighting its role in regulating CHS severity.

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Last Updated: May 20, 2026

Contact Hypersensitivity as a Murine Model of Allergic Contact Dermatitis

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The Use of Mouse Splenocytes to Assess Pathogen-associated Molecular Pattern Influence on Clock Gene Expression

The Use of Mouse Splenocytes to Assess Pathogen-associated Molecular Pattern Influence on Clock Gene Expression

Published on: July 24, 2018

Area of Science:

Immunology
Chronobiology
Dermatology

Background:

Immediate-type skin allergic reactions are linked to circadian rhythms.
The influence of circadian mechanisms on delayed-type skin allergic reactions, like contact hypersensitivity (CHS), is not well understood.
CHS is a T-cell-mediated immune response and a model for allergic contact dermatitis.

Purpose of the Study:

To investigate the impact of biological clock dysfunction on CHS pathogenesis.
To compare CHS in CLOCK mutant mice with wild-type (WT) mice.

Main Methods:

Mice were sensitized with 2,4,6-trinitro-1-chlorobenzene (TNCB) on the abdomen.
Mice were challenged with TNCB on the ears to induce CHS.
Evaluated ear swelling, serum immunoglobulin E, mast cell numbers, and corticosterone levels.

Main Results:

CLOCK mutant mice exhibited more severe inflammation, increased ear swelling, higher serum immunoglobulin E, and more mast cells compared to WT mice.
Biological clock dysfunction promoted T-helper type 2 immune responses, exacerbating CHS.
CLOCK mutation led to loss of corticosterone rhythmicity and decreased daily levels, worsening CHS. Adrenalectomy exacerbated CHS in WT mice but not CLOCK mutant mice. Dexamethasone offered greater protection in CLOCK mutant mice.

Conclusions:

Circadian rhythm plays a significant role in regulating CHS.
Corticosterone rhythmicity and levels are implicated in the circadian regulation of CHS.
CLOCK mutation disrupts corticosterone regulation, leading to exacerbated CHS.