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  Cancer-associated epithelial cell adhesion molecule (EpCAM; CD326) enables epidermal Langerhans cell motility and migration in vivo

Gaiser, M. R., Lämmermann, T., Feng, X., Igyarto, B. Z., Kaplan, D. H., Tessarollo, L., et al. (2012). Cancer-associated epithelial cell adhesion molecule (EpCAM; CD326) enables epidermal Langerhans cell motility and migration in vivo. Proceedings of the National Academy of Sciences of the United States of America, 109, E889-E897. doi:10.1073/pnas.1117674109.

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Gaiser et al..pdf (Verlagsversion), 2MB
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https://www.pnas.org/content/109/15/E889.long (Verlagsversion)
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 Urheber:
Gaiser, Maria R.1, Autor
Lämmermann, Tim2, Autor           
Feng, Xu1, Autor
Igyarto, Botond Z.1, Autor
Kaplan, Daniel H.1, Autor
Tessarollo, Lino1, Autor
Germain, Ronald N.1, Autor
Udey, and Mark C.1, Autor
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1External Organizations, ou_persistent22              
2Max Planck Institute of Immunobiology and Epigenetics, Max Planck Society, ou_1565141              

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 Zusammenfassung: After activation, Langerhans cells (LC), a distinct subpopulation of epidermis-resident dendritic cells, migrate from skin to lymph nodes where they regulate the magnitude and quality of immune responses initiated by epicutaneously applied antigens. Modulation of LC-keratinocyte adhesion is likely to be central to regulation of LC migration. LC express high levels of epithelial cell adhesion molecule (EpCAM; CD326), a cell-surface protein that is characteristic of some epithelia and many carcinomas and that has been implicated in intercellular adhesion and metastasis. To gain insight into EpCAM function in a physiologic context in vivo, we generated conditional knockout mice with EpCAM-deficient LC and characterized them. Epidermis from these mice contained increased numbers of LC with normal levels of MHC and costimulatory molecules and T-cell-stimulatory activity in vitro. Migration of EpCAM-deficient LC from skin explants was inhibited, but chemotaxis of dissociated LC was not. Correspondingly, the ability of contact allergen-stimulated, EpCAM-deficient LC to exit epidermis in vivo was delayed, and strikingly fewer hapten-bearing LC subsequently accumulated in lymph nodes. Attenuated migration of EpCAM-deficient LC resulted in enhanced contact hypersensitivity responses as previously described in LC-deficient mice. Intravital microscopy revealed reduced translocation and dendrite motility in EpCAM-deficient LC in vivo in contact allergen-treated mice. These results conclusively link EpCAM expression to LC motility/migration and LC migration to immune regulation. EpCAM appears to promote LC migration from epidermis by decreasing LC-keratinocyte adhesion and may modulate intercellular adhesion and cell movement within in epithelia during development and carcinogenesis in an analogous fashion.

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Sprache(n): eng - English
 Datum: 2012-04-10
 Publikationsstatus: Erschienen
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 Ort, Verlag, Ausgabe: -
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 Art der Begutachtung: Expertenbegutachtung
 Identifikatoren: DOI: 10.1073/pnas.1117674109
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Titel: Proceedings of the National Academy of Sciences of the United States of America
  Andere : Proc. Acad. Sci. USA
  Andere : Proc. Acad. Sci. U.S.A.
  Andere : Proceedings of the National Academy of Sciences of the USA
  Kurztitel : PNAS
Genre der Quelle: Zeitschrift
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Ort, Verlag, Ausgabe: Washington, D.C. : National Academy of Sciences
Seiten: - Band / Heft: 109 Artikelnummer: - Start- / Endseite: E889 - E897 Identifikator: ISSN: 0027-8424
CoNE: https://pure.mpg.de/cone/journals/resource/954925427230