Journal
JOURNAL OF IMMUNOLOGY
Volume 194, Issue 4, Pages 1621-1627Publisher
AMER ASSOC IMMUNOLOGISTS
DOI: 10.4049/jimmunol.1401256
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Funding
- Arthritis Research UK
- Versus Arthritis [19497] Funding Source: researchfish
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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-beta 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-beta. Inhibition of IL-6 restored the protective anti-inflammatory properties of aACs and the TGF-beta 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-beta 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-beta.
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