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논문 기본 정보

자료유형
학술저널
저자정보
Jia-Qi Chu (Affiliated Hospital of Guangdong Medical University) Ge Shi (Affiliated Hospital of Guangdong Medical University) Yi-Ming Fan (Affiliated Hospital of Guangdong Medical University) In-Wook Choi (Chungnam National University School of Medicine) Guang-Ho Cha (Chungnam National University School of Medicine) Yu Zhou (Affiliated Hospital of Guangdong Medical University) Young-Ha Lee (Chungnam National University School of Medicine) Juan-Hua Quan (Affiliated Hospital of Guangdong Medical University)
저널정보
대한기생충학열대의학회 Parasites, Hosts and Diseases The Korean Journal of Parasitology Vol.54 No.6
발행연도
2016.12
수록면
711 - 717 (7page)

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Toxoplasma gondii is an obligate intracellular parasite that stimulates production of high levels of proinflammatory cytokines, which are important for innate immunity. NLRs, i.e., nucleotide-binding oligomerization domain (NOD)-like receptors, play a crucial role as innate immune sensors and form multiprotein complexes called inflammasomes, which mediate caspase-1-dependent processing of pro-IL-1β. To elucidate the role of inflammasome components in T. gondii-infected THP-1 macrophages, we examined inflammasome-related gene expression and mechanisms of inflammasome-regulated cytokine IL-1β secretion. The results revealed a significant upregulation of IL-1β after T. gondii infection. T. gondii infection also upregulated the expression of inflammasome sensors, including NLRP1, NLRP3, NLRC4, NLRP6, NLRP8, NLRP13, AIM2, and NAIP, in a time-dependent manner. The infection also upregulated inflammasome adaptor protein ASC and caspase-1 mRNA levels. From this study, we newly found that T. gondii infection regulates NLRC4, NLRP6, NLRP8, NLRP13, AIM2, and neuronal apoptosis inhibitor protein (NAIP) gene expressions in THP-1 macrophages and that the role of the inflammasome-related genes may be critical for mediating the innate immune responses to T. gondii infection.

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Abstract
INTRODUCTION
MATERIALS AND METHODS
RESULTS
DISCUSSION
REFERENCES

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UCI(KEPA) : I410-ECN-0101-2017-513-002126442