NDLI: Cutting edge: Endoplasmic reticulum stress licenses macrophages to produce mature IL-1ß in response to TLR4 stimulation through a caspase-8- and TRIF-dependent pathway.

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Cutting edge: Endoplasmic reticulum stress licenses macrophages to produce mature IL-1ß in response to TLR4 stimulation through a caspase-8- and TRIF-dependent pathway.

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Cutting edge: Endoplasmic reticulum stress licenses macrophages to produce mature IL-1ß in response to TLR4 stimulation through a caspase-8- and TRIF-dependent pathway.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Shenderov, Kevin Dillon, Christopher P. Cerundolo, Vincenzo Hieny, Sara Yip, Ronald Riteau, Nicolas Fitzgerald, Pat Oberst, Andrew Oland, Sandy Mayer-Barber, Katrin D. Green, Douglas R. Sher, Alan
Description	Author Affiliation: Shenderov K ( Immunobiology Section, Laboratory of Parasitic Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892)
Abstract	The accumulation of improperly folded proteins within the endoplasmic reticulum (ER) generates perturbations known as ER stress that engage the unfolded protein response. ER stress is involved in many inflammatory pathologies that are also associated with the production of the proinflammatory cytokine IL-1ß. In this study, we demonstrate that macrophages undergoing ER stress are able to drive the production and processing of pro-IL-1ß in response to LPS stimulation in vitro. Interestingly, the classical NLRP3 inflammasome is dispensable, because maturation of pro-IL-1ß occurs normally in the absence of the adaptor protein ASC. In contrast, processing of pro-IL-1ß is fully dependent on caspase-8. Intriguingly, we found that neither the unfolded protein response transcription factors XBP1 and CHOP nor the TLR4 adaptor molecule MyD88 is necessary for caspase-8 activation. Instead, both caspase activation and IL-1ß production require the alternative TLR4 adaptor TRIF. This pathway may contribute to IL-1-driven tissue pathology in certain disease settings.
ISSN	00221767
e-ISSN	15506606
DOI	10.4049/jimmunol.1302549
Journal	The Journal of Immunology
Issue Number	5
Volume Number	192
Language	English
Publisher	The American Association of Immunologists
Publisher Date	2014-03-01
Publisher Place	United States
Access Restriction	Open
Subject Keyword	Adaptor Proteins, Vesicular Transport Immunology Caspase 8 Metabolism Endoplasmic Reticulum Stress Physiology Interleukin-1beta Macrophages Toll-like Receptor 4 Genetics Animals Dna-binding Proteins Enzyme Activation Inflammation Cytology Mice Mice, Knockout Myeloid Differentiation Factor 88 Transcription Factor Chop Transcription Factors Unfolded Protein Response Research Support, N.i.h., Intramural Research Support, Non-u.s. Gov't Discipline Immunology
Content Type	Text
Resource Type	Article
Subject	Immunology and Allergy Immunology

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