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Published on: January 26, 2016
Epidermal langerhans cell-deficient mice develop enhanced contact hypersensitivity
Daniel H Kaplan1, Mathew C Jenison, Sem Saeland
1Department of Dermatology, Yale University School of Medicine, New Haven, Connecticut 06520, USA. dan.kaplan@yale.edu
Insights
Epidermal Langerhans cells (LCs) are not essential for skin immunity and contact hypersensitivity (CHS). Their absence unexpectedly amplifies CHS, revealing a previously unknown regulatory role in immune responses.
Area of Science:
- Immunology
- Dermatology
- Cell Biology
Background:
- Epidermal Langerhans cells (LCs) are skin-resident dendritic cells crucial for initiating adaptive immunity.
- Their precise role in skin immunity, particularly in contact hypersensitivity (CHS), remains incompletely understood.
Purpose of the Study:
- To investigate the functional requirement of LCs in skin immunity.
- To elucidate the role of LCs in the development of contact hypersensitivity.
Main Methods:
- Generation of BAC transgenic mice with targeted ablation of epidermal LCs using diphtheria toxin.
- Assessment of contact hypersensitivity responses in LCs-deficient mice.
Main Results:
- Absence of epidermal LCs resulted in amplified, not abrogated, contact hypersensitivity responses.
- LCs were found to regulate the priming phase of CHS, not the effector phase.
- LCs demonstrated a previously unappreciated function in regulating immune responses.
Conclusions:
- Epidermal LCs are dispensable for CHS.
- LCs play a regulatory role in immune responses, specifically during the priming phase of CHS.
- These findings challenge the established view of LCs' primary function in initiating adaptive immunity.
Abstract:
Epidermal Langerhans cells (LCs), a distinct skin-resident dendritic cell population, acquire antigen in the skin and migrate to draining lymph nodes where they are thought to initiate adaptive immune responses. To examine the functional requirement of LCs in skin immunity, we generated BAC transgenic mice in which the regulatory elements from human Langerin were used to drive expression of diphtheria toxin. The resulting mice have a constitutive and durable absence of epidermal LCs but are otherwise intact. Unexpectedly, we found that contact hypersensitivity (CHS) was amplified rather than abrogated in the absence of LCs. Moreover, we showed that LCs act during the priming and not the effector phase. Thus, LCs not only were dispensable for CHS, but they served to regulate the response, a previously unappreciated function.
