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Engulfment of activated apoptotic cells abolishes TGF-β-mediated immunoregulation via the induction of IL-6.

Authors
  • Notley, Clare A
  • Brown, Mark A
  • McGovern, Jenny L
  • Jordan, Christine K
  • Ehrenstein, Michael R
Type
Published Article
Journal
The Journal of Immunology
Publisher
The American Association of Immunologists
Publication Date
Feb 15, 2015
Volume
194
Issue
4
Pages
1621–1627
Identifiers
DOI: 10.4049/jimmunol.1401256
PMID: 25601923
Source
Medline
License
Unknown

Abstract

Phagocytosis of apoptotic cells (ACs) is usually a potent immunoregulatory signal but can also promote inflammation. In this article, we show that administration of apoptotic dendritic cells (DCs) inhibited inflammation in vivo through increasing production of TGF-β from intrinsic DCs and B cells. However, ACs derived from LPS-activated DCs failed to restrain inflammation because of a short-lived but marked IL-6 response, which abolished the increase in TGF-β. Inhibition of IL-6 restored the protective anti-inflammatory properties of aACs and the TGF-β response. DCs isolated from mice that had received resting but not activated ACs could transfer the suppression of inflammation to recipient mice. These transferred DCs stimulated B cell TGF-β production and relied on an intact B cell compartment to limit inflammation. These results highlight how the activation state of AC governs their ability to control inflammation through reciprocal regulation of IL-6 and TGF-β.

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