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Differential regulation of toll-like receptor-mediated cytokine production by unfolded protein response

Cited 5 time in Web of Science Cited 7 time in Scopus
Authors
Kim, Sena; Joe, Yeonsoo; Surh, Young-Joon; Chung, Hun Taeg
Issue Date
2018-01
Citation
Oxidative Medicine and Cellular Longevity, Vol.2018, p. 9827312
Abstract
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-3 beta. 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
URI
https://hdl.handle.net/10371/172882
DOI
https://doi.org/10.1155/2018/9827312
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Graduate School of Convergence Science and Technology (융합과학기술대학원)Dept. of Molecular and Biopharmaceutical Sciences (분자의학 및 바이오제약학과)Journal Papers (저널논문_분자의학 및 바이오제약학과)
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