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Blood. 2011 Apr 7;117(14):3793-8. doi: 10.1182/blood-2010-11-318832. Epub 2011 Feb 16.

Serum amyloid A overrides Treg anergy via monocyte-dependent and Treg-intrinsic, SOCS3-associated pathways.

Author information

1
Department of Pediatrics, Immunology Program, Stanford University School of Medicine, 259 Campus Drive, Stanford, CA 94305, USA. kdnguyen@stanford.edu

Abstract

The acute phase protein serum amyloid A (SAA) has been well characterized as an indicator of inflammation. Nevertheless, its functions in pro versus anti-inflammatory processes remain obscure. Here we provide unexpected evidences that SAA induces the proliferation of the tolerogenic subset of regulatory T cells (T(reg)). Intriguingly, SAA reverses T(reg) anergy via its interaction with monocytes to activate distinct mitogenic pathways in T(reg) but not effector T cells. This selective responsiveness of T(reg) correlates with their diminished expression of SOCS3 and is antagonized by T(reg)-specific induction of this regulator of cytokine signaling. Collectively, these evidences suggest a novel anti-inflammatory role of SAA in the induction of a micro-environment that supports T(reg) expansion at sites of infection or tissue injury, likely to curb (auto)-inflammatory responses.

PMID:
21325601
PMCID:
PMC3296631
DOI:
10.1182/blood-2010-11-318832
[Indexed for MEDLINE]
Free PMC Article

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