Immunomodulatory cross-talk between conjunctival goblet cells and dendritic cells.

Goblet cells are secretory epithelial cells of mucosal tissues that confer protection from environmental agents or pathogens via expression and secretion of soluble mucins. Loss of these cells is associated with several chronic inflammatory disorders of the mucosa. Although demonstrated to transfer...

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Main Authors: Laura Contreras-Ruiz, Sharmila Masli
Format: Article
Language:English
Published: Public Library of Science (PLoS) 2015-01-01
Series:PLoS ONE
Online Access:http://europepmc.org/articles/PMC4368435?pdf=render
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spelling doaj-f4fdaf2dbbff44c483b34123c0379b8b2020-11-25T00:19:16ZengPublic Library of Science (PLoS)PLoS ONE1932-62032015-01-01103e012028410.1371/journal.pone.0120284Immunomodulatory cross-talk between conjunctival goblet cells and dendritic cells.Laura Contreras-RuizSharmila MasliGoblet cells are secretory epithelial cells of mucosal tissues that confer protection from environmental agents or pathogens via expression and secretion of soluble mucins. Loss of these cells is associated with several chronic inflammatory disorders of the mucosa. Although demonstrated to transfer antigens from the luminal surface to stromal cells in the intestinal mucosa, it is not known if goblet cells contribute to the regulation of an immune response. In this study we report that similar to intestinal and respiratory mucosal epithelia, mouse ocular surface epithelia predominantly express the TGF-ß2 isoform. Specifically, we demonstrate the ability of goblet cells to express TGF-ß2 and increase it in response to Toll-Like Receptor 4 mediated stimulus in cultures. Goblet cells not only express TGF-ß2, but are also able to activate it in a thrombospondin-1 (TSP-1) dependent manner via their cell surface receptor CD36. Furthermore, goblet cell derived soluble factors that possibly include TGF-ß2, alter dendritic cell (DC) phenotype to a tolerogenic type by downregulating DC expression of MHC class II and co-stimulatory molecules CD80, CD86 and CD40. Thus our study demonstrates goblet cells as a cellular source of active TGF-ß2 in ocular mucosa and implicates their immunomodulatory function in maintaining mucosal immune homeostasis.http://europepmc.org/articles/PMC4368435?pdf=render
collection DOAJ
language English
format Article
sources DOAJ
author Laura Contreras-Ruiz
Sharmila Masli
spellingShingle Laura Contreras-Ruiz
Sharmila Masli
Immunomodulatory cross-talk between conjunctival goblet cells and dendritic cells.
PLoS ONE
author_facet Laura Contreras-Ruiz
Sharmila Masli
author_sort Laura Contreras-Ruiz
title Immunomodulatory cross-talk between conjunctival goblet cells and dendritic cells.
title_short Immunomodulatory cross-talk between conjunctival goblet cells and dendritic cells.
title_full Immunomodulatory cross-talk between conjunctival goblet cells and dendritic cells.
title_fullStr Immunomodulatory cross-talk between conjunctival goblet cells and dendritic cells.
title_full_unstemmed Immunomodulatory cross-talk between conjunctival goblet cells and dendritic cells.
title_sort immunomodulatory cross-talk between conjunctival goblet cells and dendritic cells.
publisher Public Library of Science (PLoS)
series PLoS ONE
issn 1932-6203
publishDate 2015-01-01
description Goblet cells are secretory epithelial cells of mucosal tissues that confer protection from environmental agents or pathogens via expression and secretion of soluble mucins. Loss of these cells is associated with several chronic inflammatory disorders of the mucosa. Although demonstrated to transfer antigens from the luminal surface to stromal cells in the intestinal mucosa, it is not known if goblet cells contribute to the regulation of an immune response. In this study we report that similar to intestinal and respiratory mucosal epithelia, mouse ocular surface epithelia predominantly express the TGF-ß2 isoform. Specifically, we demonstrate the ability of goblet cells to express TGF-ß2 and increase it in response to Toll-Like Receptor 4 mediated stimulus in cultures. Goblet cells not only express TGF-ß2, but are also able to activate it in a thrombospondin-1 (TSP-1) dependent manner via their cell surface receptor CD36. Furthermore, goblet cell derived soluble factors that possibly include TGF-ß2, alter dendritic cell (DC) phenotype to a tolerogenic type by downregulating DC expression of MHC class II and co-stimulatory molecules CD80, CD86 and CD40. Thus our study demonstrates goblet cells as a cellular source of active TGF-ß2 in ocular mucosa and implicates their immunomodulatory function in maintaining mucosal immune homeostasis.
url http://europepmc.org/articles/PMC4368435?pdf=render
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