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Physiological role of TNF in mucosal immunology : Regulation of macrophage/dendritic cell function

Rivollier, Aymeric LU ; Marsal, Jan LU and Agace, William W. LU (2015) In Anti-Tumor Necrosis Factor Therapy in Inflammatory Bowel Disease p.9-26
Abstract

Intestinal mononuclear phagocytes, comprising macrophages (MΦs) and dendritic cells (DCs), play important roles in the generation and the regulation of immune responses to intestinal antigens, and alterations in the development and/or the function of these cells are thought to contribute to the pathogenesis of inflammatory bowel disease. In this review, we discuss the role of tumor necrosis factor-a (TNF) in regulating multiple aspects of intestinal M? and DC physiology, including their differentiation, migration, maturation, survival and effector functions. In inflammatory bowel disease, TNF signaling has been implicated in reprogramming monocyte differentiation from the anti-inflammatory MΦ lineage towards the pro-inflammatory... (More)

Intestinal mononuclear phagocytes, comprising macrophages (MΦs) and dendritic cells (DCs), play important roles in the generation and the regulation of immune responses to intestinal antigens, and alterations in the development and/or the function of these cells are thought to contribute to the pathogenesis of inflammatory bowel disease. In this review, we discuss the role of tumor necrosis factor-a (TNF) in regulating multiple aspects of intestinal M? and DC physiology, including their differentiation, migration, maturation, survival and effector functions. In inflammatory bowel disease, TNF signaling has been implicated in reprogramming monocyte differentiation from the anti-inflammatory MΦ lineage towards the pro-inflammatory mononuclear phagocyte lineage. These cells become a major source of TNF and, thus, may contribute to the chronic inflammatory process. Finally, we highlight some of the important gaps in our current knowledge regarding the role of TNF in MΦ and DC physiology and suggest important directions for future research in this field.

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author
organization
publishing date
type
Chapter in Book/Report/Conference proceeding
publication status
published
subject
in
Anti-Tumor Necrosis Factor Therapy in Inflammatory Bowel Disease
pages
18 pages
publisher
S. Karger AG
external identifiers
  • scopus:84960309968
DOI
10.1159/000381381
language
English
LU publication?
yes
id
ff53ae00-dfae-4a3f-8a95-2730b716d62a
date added to LUP
2016-09-23 11:48:50
date last changed
2017-01-01 08:34:56
@inbook{ff53ae00-dfae-4a3f-8a95-2730b716d62a,
  abstract     = {<p>Intestinal mononuclear phagocytes, comprising macrophages (MΦs) and dendritic cells (DCs), play important roles in the generation and the regulation of immune responses to intestinal antigens, and alterations in the development and/or the function of these cells are thought to contribute to the pathogenesis of inflammatory bowel disease. In this review, we discuss the role of tumor necrosis factor-a (TNF) in regulating multiple aspects of intestinal M? and DC physiology, including their differentiation, migration, maturation, survival and effector functions. In inflammatory bowel disease, TNF signaling has been implicated in reprogramming monocyte differentiation from the anti-inflammatory MΦ lineage towards the pro-inflammatory mononuclear phagocyte lineage. These cells become a major source of TNF and, thus, may contribute to the chronic inflammatory process. Finally, we highlight some of the important gaps in our current knowledge regarding the role of TNF in MΦ and DC physiology and suggest important directions for future research in this field.</p>},
  author       = {Rivollier, Aymeric and Marsal, Jan and Agace, William W.},
  language     = {eng},
  month        = {07},
  pages        = {9--26},
  publisher    = {S. Karger AG},
  series       = {Anti-Tumor Necrosis Factor Therapy in Inflammatory Bowel Disease},
  title        = {Physiological role of TNF in mucosal immunology : Regulation of macrophage/dendritic cell function},
  url          = {http://dx.doi.org/10.1159/000381381},
  year         = {2015},
}