title: Soluble CD93 induces differentiation of monocytes and enhances TLR responses.
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.
authors.affiliation: Nucleic Acid Biochemistry Laboratory, Department of Biological Science, Graduate School of Medical Science and Engineering, Korea Advanced Institute of Science and Technology, Daejeon, Korea.
authors.forename: Jae-Won
authors.initials: JW
authors.lastname: Jeon
authors.forename: Joon-Goo
authors.initials: JG
authors.lastname: Jung
authors.forename: Eui-Cheol
authors.initials: EC
authors.lastname: Shin
authors.forename: Hye In
authors.initials: HI
authors.lastname: Choi
authors.forename: Ho Youn
authors.initials: HY
authors.lastname: Kim
authors.forename: Mi-La
authors.initials: ML
authors.lastname: Cho
authors.forename: Sun-Wha
authors.initials: SW
authors.lastname: Kim
authors.forename: Young-Soon
authors.initials: YS
authors.lastname: Jang
authors.forename: Myung-Ho
authors.initials: MH
authors.lastname: Sohn
authors.forename: Ji-Hyun
authors.initials: JH
authors.lastname: Moon
authors.forename: Young-Hun
authors.initials: YH
authors.lastname: Cho
authors.forename: Kwang-Lae
authors.initials: KL
authors.lastname: Hoe
authors.forename: Yeon-Soo
authors.initials: YS
authors.lastname: Seo
authors.forename: Young Woo
authors.initials: YW
authors.lastname: Park
mesh_terms: D001172:Arthritis, Rheumatoid / Q000276:immunology / Q000378:metabolism; D002454:Cell Differentiation / Q000276:immunology*; D016207:Cytokines / Q000096:biosynthesis; D004797:Enzyme-Linked Immunosorbent Assay; D006801:Humans; D007249:Inflammation / Q000276:immunology / Q000378:metabolism; D008562:Membrane Glycoproteins / Q000276:immunology / Q000378:metabolism*; D009000:Monocytes / Q000166:cytology* / Q000276:immunology / Q000378:metabolism; D011951:Receptors, Complement / Q000276:immunology / Q000378:metabolism*; D011994:Recombinant Proteins; D020133:Reverse Transcriptase Polymerase Chain Reaction; D013582:Synovial Fluid / Q000276:immunology / Q000378:metabolism; D051193:Toll-Like Receptors / Q000276:immunology / Q000378:metabolism*
chemical_list: D016207:Cytokines; D008562:Membrane Glycoproteins; D011951:Receptors, Complement; D011994:Recombinant Proteins; D051193:Toll-Like Receptors; C032402:complement 1q receptor