ID | 32882 |
JaLCDOI | |
フルテキストURL | |
著者 |
Yano, Ryusuke
Okayama University
Yamanura, Masahiro
Okayama University
Sunahori, Katsue
Okayama University
Takasugi, Kouji
Okayama University
Yamana, Jiro
Okayama University
Kawashima, Masanori
Okayama University
Makino, Hirofumi
Okayama University
|
抄録 | CD16+ monocytes, identified as a minor population of monocytes in human peripheral blood, have been implicated in several inflammatory diseases, including rheumatoid arthritis (RA). Fractalkine (FKN, CX3CL1), a member of the CX3 C subfamily, is induced by pro-inflammatory cytokines, while a receptor for FKN, CX3CR1, is capable of mediating both leukocyte migration and firm adhesion. Here, we investigated the role of FKN and CX3CR1 in activation of CD16+ monocytes and their recruitment into synovial tissues in RA patients. High levels of soluble FKN were detected in the synovial fluid and sera of RA patients. Circulating CD16+ monocytes showed a higher level of CX3CR1 expression than CD16- monocytes in both RA patients and healthy subjects. High level expression of CX3CR1 was also seen in CD16+ monocytes localized to the lining layer in RA synovial tissue. In the in vitro culture experiments, IL-10 induced CX3CR1 expression on the surface of monocytes, and TNFalpha induced membrane-bound FKN as well as soluble FKN expression in synovial fibroblasts. Moreover, soluble FKN was capable of inducing IL-1beta and IL-6 by activated monocytes. These results suggest that FKN might preferentially mediate migration and recruitment of CD16+ monocytes, and might contribute to synovial tissue inflammation. |
キーワード | CD16
monocytes
fractalkine
CX3CR1
rheumatoid arthritis
|
Amo Type | Original Article
|
出版物タイトル |
Acta Medica Okayama
|
発行日 | 2007-04
|
巻 | 61巻
|
号 | 2号
|
出版者 | Okayama University Medical School
|
開始ページ | 89
|
終了ページ | 98
|
ISSN | 0386-300X
|
NCID | AA00508441
|
資料タイプ |
学術雑誌論文
|
言語 |
英語
|
論文のバージョン | publisher
|
査読 |
有り
|
PubMed ID | |
Web of Science KeyUT |