Differential Regulation of Toll-Like Receptor-Mediated Cytokine Production by Unfolded Protein Response

The ability of the host immune response is largely mediated by the proinflammatory cytokine production. Physiological and pathological conditions of endoplasmic reticulum (ER) trigger unfolded protein response and contribute to the development or pathology of inflammatory diseases. Under ER stress,...

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Bibliographic Details
Published in:Oxidative medicine and cellular longevity 2018-01, Vol.2018 (2018), p.1-8
Main Authors: Chung, Hun Taeg, Surh, Young-Joon, Joe, Yeonsoo, Kim, Sena
Format: Article
Language:English
Subjects:
Apoptosis
Cytokines
Cytokines - metabolism
Diabetes
Endoplasmic reticulum
Endoplasmic Reticulum Stress
Enzymes
Glycogen Synthase Kinase 3 beta - metabolism
Homeostasis
Humans
Immune response
Immunology
Inflammasomes - metabolism
Inflammation
Kinases
Metabolism
Mitogen-Activated Protein Kinases - metabolism
NF-kappa B - metabolism
Proteins
Regulation
Review
Rodents
Signal Transduction
Stress response
Toll-Like Receptors - metabolism
Transcription factors
Unfolded Protein Response
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Summary:The ability of the host immune response is largely mediated by the proinflammatory cytokine production. Physiological and pathological conditions of endoplasmic reticulum (ER) trigger unfolded protein response and contribute to the development or pathology of inflammatory diseases. Under ER stress, unfolded protein response (UPR) signaling pathways participate in upregulating inflammatory cytokine production via NF-kappaB, MAPK, and GSK-3β. Moreover, it has been suggested that ER stress crosstalks with toll-like receptor (TLR) signaling pathway to promote the production of proinflammatory cytokines. In addition, TLR stimulation can lead to UPR activation to promote inflammation. In this review, we will cover how proinflammatory cytokine production by UPR signaling can be induced or amplified in the presence or absence of TLR activation.
ISSN:1942-0900
1942-0994
DOI:10.1155/2018/9827312