Soluble CD93 induces differentiation of monocytes and enhances TLR responses = 수용성 CD93에 의한 monocyte의 분화 와 TLR 반응 증가

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Title
Soluble CD93 induces differentiation of monocytes and enhances TLR responses = 수용성 CD93에 의한 monocyte의 분화 와 TLR 반응 증가
Author(s)
Jae Won Jeon; Joon Goo Jeong; E C Shin; H I Choi; H Y Kim; M L Cho; S W Kim; Young Soon Jang; Myung Ho Sohn; Ji-hyun Moon; Y H Cho; Kwang Lae Hoe; Y S Seo; Young Woo Park
Bibliographic Citation
Journal of Immunology, vol. 185, no. 8, pp. 4921-4927
Publication Year
2010
Abstract
The cell surface protein CD93 is known to be involved in the regulation of phagocytosis and cell adhesion. Although typically membrane-bound, a soluble form of CD93 (sCD93) has recently been identified. Currently, however, the role of sCD93 in monocyte function is unknown. In the current study, we analyzed the functional effects of sCD93 on THP-1 monocytic cells and human primary monocytes. Various forms of recombinant human sCD93 were used to investigate the effects of this molecule on both human primary monocytes and a monocytic cell line, THP-1. We found that sCD93 induced differentiation of monocytes to macrophage-like cells, as evidenced by activated cell adhesion and increased phagocytic activities. In addition, this differentiation resulted in an enhanced response to TLR stimulation in terms of differentiation marker expression and proinflammatory cytokine production. Furthermore, sCD93 enhanced LPS-stimulated TNF-α production even prior to monocyte differentiation. To investigate a possible role for sCD93 in the pathogenesis of chronic inflammatory diseases, we assessed the concentration of sCD93 in synovial fluid from patients with rheumatoid arthritis and found it to be significantly increased compared with synovial fluid from patients with osteoarthritis. Together, these data revealed a function for sCD93 that may have implications in inflammation and inflammatory diseases including rheumatoid arthritis.
ISSN
0022-1767
Publisher
Amer Assoc Immunologists
DOI
http://dx.doi.org/10.4049/jimmunol.0904011
Type
Article
Appears in Collections:
1. Journal Articles > Journal Articles
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