期刊
JOURNAL OF INVESTIGATIVE DERMATOLOGY
卷 140, 期 1, 页码 132-+出版社
ELSEVIER SCIENCE INC
DOI: 10.1016/j.jid.2019.06.132
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资金
- Landsteiner Foundation for Blood Transfusion Research (LSBR), the Netherlands [0414F]
- Netherlands Organisation for Scientific Research (NWO), the Netherlands [VIDI 917-76-365]
- German Science Foundation (DFG), Germany [CL 419/2-1]
The cell adhesion molecule E-cadherin is a major component of adherens junctions and marks Langerhans cells (LC), the only dendritic cell (DC) population of the epidermis. LC form a dense network and attach themselves to the surrounding keratinocytes via homophilic E-cadherin binding. LC activation, mobilization, and migration require a reduction in LC E-cadherin expression. To determine whether E-cadherin plays a role in regulating LC homeostasis and function, we generated CD11c-specific E-cadherin knockout mice (CD11c-Ecad(del)). In the absence of E-cadherin-mediated cell adhesion, LC numbers remained stable and similar as in control mice, even in aged animals. Intriguingly, E-cadherin-deficient LC displayed a dramatically changed morphology characterized by a more rounded cell body and fewer dendrites than wild-type cells. Nevertheless, maturation and migration of LC lacking E-cadherin was not altered, neither under steady-state nor inflammatory conditions. Accordingly, CD11c-Ecad(del) and control mice developed comparable contact hypersensitivity reactions and imiquimod-triggered psoriatic skin inflammation, indicating that E-cadherin on LC does not influence their ability to orchestrate T cell-mediated immunity. In conclusion, our data demonstrate that E-cadherin is dispensable to maintain LC in the epidermis and does not regulate LC maturation, migration, and function.
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