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Turning down the heat: the potential role of RIP140 in inflammation

Cellular & Molecular Immunology volume 9, pages 195–196 (2012)Cite this article

The control of inflammation is an essential process for maintaining immune homeostasis, but the regulatory mechanisms which govern this event remain poorly understood. Endotoxin tolerance is a convenient experimental model which can be used to elucidate potentially relevant mechanisms that control the host's inflammatory response. Endotoxin tolerance is marked by a transitory period of hyporesponsiveness to lipopolysaccharide (LPS, also known as endotoxin) stimulation following an initial exposure to LPS. Although the alteration of intracellular signaling has been well described, there are likely multiple mechanisms and pathways which contribute to the phenomenon called endotoxin tolerance.

In the April issue of Nature Immunology, a role for the nuclear receptor corepressor, named receptor-interacting protein 140 (RIP140), is introduced as another potentially important molecular mechanism in modulating the inflammatory response.1 Using an experimental model of endotoxin tolerance, the authors show that RIP140 regulates the transcription and production of NF-κB-dependent pro-inflammatory cytokines.

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Authors and Affiliations

  1. Center for Vaccine Development, University of Maryland School of Medicine, Baltimore, MD, USA

    Wilbur H Chen

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  1. Wilbur H Chen
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Correspondence to Wilbur H Chen.

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Chen, W. Turning down the heat: the potential role of RIP140 in inflammation. Cell Mol Immunol 9, 195–196 (2012). https://doi.org/10.1038/cmi.2012.9

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