Apicobasal polarity controls lymphocyte adhesion to hepatic epithelial cells
Publisher
ElsevierDate
2014-01-01Citation
10.1016/j.celrep.2014.08.007
Cell Reports 8 (2014): 1879–1893
ISSN
2211-1247DOI
10.1016/j.celrep.2014.08.007Funded by
This work was supported by grants SAF2011-22624 (to J.M.), BFU2012-32532 and CSD2009-00016 (to M.A.A.), and BFU2011- 22859 (to I.C.) from the Ministerio de Ciencia e Innovación; grant S2010/ BMD-2305 from Comunidad de Madrid; and grant FIS PI10/00101 from the Ministerio Sanidad and Fundacio n Mutua Madrileña (to P.L.). N.R. is a recipient of a JAE predoctoral fellowship from the CSIC. B.M. is a recipient of an FPI fellowship from the MINECOProject
Comunidad de Madrid. S2010/BMD-2305/CS INTERATOMICSSubjects
Apicobasal; ICAM-1; Epithelial cells; Biología y Biomedicina / BiologíaRights
© 2014 The AuthorsEsta obra está bajo una licencia de Creative Commons Reconocimiento-NoComercial-SinObraDerivada 4.0 Internacional.
Abstract
Loss of apicobasal polarity is a hallmark of epithelial
pathologies. Leukocyte infiltration and crosstalk with
dysfunctional epithelial barriers are crucial for the inflammatory
response. Here, we show that apicobasal
architecture regulates the adhesion between hepatic
epithelial cells and lymphocytes. Polarized hepatocytes
and epithelium from bile ducts segregate the
intercellular adhesion molecule 1 (ICAM-1) adhesion
receptor onto their apical, microvilli-rich membranes,
which are less accessible by circulating immune
cells. Upon cell depolarization, hepatic ICAM-1 becomes
exposed and increases lymphocyte binding.
Polarized hepatic cells prevent ICAM-1 exposure
to lymphocytes by redirecting basolateral ICAM-1
to apical domains. Loss of ICAM-1 polarity occurs
in human inflammatory liver diseases and can be
induced by the inflammatory cytokine tumor necrosis
factor alpha (TNF-a). We propose that adhesion
receptor polarization is a parenchymal immune
checkpoint that allows functional epithelium to
hamper leukocyte binding. This contributes to the
haptotactic guidance of leukocytes toward neighboring
damaged or chronically inflamed epithelial
cells that expose their adhesion machinery
Files in this item
Google Scholar:Reglero-Real, Natalia
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Álvarez-Varela, Adrián
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Cernuda-Morollón, Eva
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Feito, Jorge
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Marcos-Ramiro, Beatriz
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Fernández-Martín, Laura
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Gómez-Lechón, Maria José
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Muntané, Jordi
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Sandoval, Pilar
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Majano Rodríguez, Pedro Lorenzo
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Correas Hornero, María Isabel
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Alonso, Miguel Angel
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Millán, Jaime
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