Recruitment of CD16+ monocytes into synovial tissues is mediated by fractalkine and CX3CR1 in rheumatoid arthritis patients

Ryusuke Yano, Masahiro Yamamura, Katsue Sunahori, Kouji Takasugi, Jiro Yamana, Masanori Kawashima, Hirofumi Makino

Research output: Contribution to journalArticlepeer-review

53 Citations (Scopus)


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 TNFα induced membrane-bound FKN as well as soluble FKN expression in synovial fibroblasts. Moreover, soluble FKN was capable of inducing IL-1β 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. Copyright

Original languageEnglish
Pages (from-to)89-98
Number of pages10
JournalActa medica Okayama
Issue number2
Publication statusPublished - Apr 2007


  • CD16
  • CX3CR1
  • Fractalkine
  • Monocytes
  • Rheumatoid arthritis

ASJC Scopus subject areas

  • Biochemistry, Genetics and Molecular Biology(all)


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