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Increased IL-6 expression on THP-1 by IL-34 stimulation up-regulated rheumatoid arthritis Th17 cells.

Abstract：

:IL-34 is a pleiotropic cytokine, which is a key regulator of monocytes/macrophages and might participate in the pathogenesis of RA. In this study, we aimed to explore the effect of IL-34 on the monocyte-like cell line THP-1 and the quantitative variation of Th17 cells in THP-1 and RA CD4+T cells coculture system. CD4+T cells were purified from RA PBMC using immunomagnetic beads. THP-1 were cultured with RA CD4+T cells. The frequency of Th17 cells was determined by FACS. Fluorscence indensity and expression of ROS were detected by FACS and cell staining, respectively. The expression of IL-6, IL-23, IL-21, TNF-α and IL-1β in the coculture supernatants were detected by ELISA. We found that CSF-1R was constitutively expressed on peripheral monocytes as well as THP-1, but not on the T/B cells. IL-34-CSF-1R binding could activate THP-1 to secret IL-6. IL-34 could up-regulate the numbers of Th17 cells in coculture system, which was possibly via the production of IL-6. We further observed ROS levels were increased in the coculture system. The percentage of Th17 cells was reduced when ROS production was inhibited by NAC, a specific inhibitor of ROS production. In addition, TNFRII antagonist but not IL-1βR antagonist could restrict the production of ROS, expression of IL-6 and generation of Th17 cells. In conclusion, IL-34-stimulated THP-1 can produce higher levels of ROS, which promoted IL-6 secretion and up-regulated Th17 cells. Our study suggests a novel mechanistic insight into how the interaction of IL-34-stimulated monocytes and CD4+T cells participates in the RA pathogenesis.

journal_name

Clin Rheumatol

journal_title

Clinical rheumatology

authors

Wang B,Tang Y,Sun X,Ouyang X,Li H,Wei J,Zhang Y,Li X

doi

10.1007/s10067-017-3746-y

subject

Has Abstract

pub_date

2018-01-01 00:00:00

pages

127-137

issue

1

eissn

0770-3198

issn

1434-9949

pii

10.1007/s10067-017-3746-y

journal_volume

37

pub_type

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