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Ribosomal Protein L19 and L22 Modulate TLR3 Signaling

Authors
 Eun-Jeong Yang  ;  Jin-Won Seo  ;  In-Hong Choi 
Citation
 IMMUNE NETWORK, Vol.11(3) : 155-162, 2011 
Journal Title
IMMUNE NETWORK
ISSN
 1598-2629 
Issue Date
2011
Keywords
RPL19 ; RPL22 ; TLR3
Abstract
BACKGROUND: Toll-like receptor 3 (TLR3) recognizes double-stranded RNA (dsRNA) and induces inflammation. In this study we attempted to ascertain if there are endogenous host molecules controlling the production of cytokines and chemokines. Two candidates, ribosomal protein L19 and L22, were analyzed to determine if they influence cytokine production followed by TLR3 activation. In this study we report that L19 acts upon production of IP-10 or IL-8 differently in glioblastoma cells.

METHODS: L19 or L22 was transfected into HEK293-TLR3, A549 or A172 cells. After treatment with several inhibitors of NF-kB, PI3K, p38 or ERK, production of IL-8 or IP-10 was measured by ELISA. siRNA was introduced to suppress expression of L19. After Vesicular stomatitis virus infection, viral multiplication was measured by western blot.

RESULTS: L19 increased ERK activation to produce IL-8. In A172 cells, in which TLR3 is expressed at endosomes, L19 inhibited interferon regulatory factor 3 (IRF3) activation and IP-10 production to facilitate viral multiplication, whereas L19 inhibited viral multiplication in A549 cells bearing TLR3 on their cell membrane.

CONCLUSION: Our results suggest that L19 regulates TLR3 signaling, which is cell type specific and may be involved in pathogenesis of autoimmune diseases and chronic inflammatory diseases.
Files in This Item:
T201103226.pdf Download
DOI
10.4110/in.2011.11.3.155
Appears in Collections:
1. College of Medicine (의과대학) > Dept. of Microbiology (미생물학교실) > 1. Journal Papers
Yonsei Authors
Seo, Jin Won(서진원)
Yang, Eun Jeong(양은정) ORCID logo https://orcid.org/0000-0003-3516-1229
Choi, In Hong(최인홍) ORCID logo https://orcid.org/0000-0001-9851-0137
URI
https://ir.ymlib.yonsei.ac.kr/handle/22282913/94069
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