Preferential Induction of the t cell auxiliary signaling molecule B7-H3 on synovial monocytes in rheumatoid arthritis

Bo Ruem Yoon, Yeon Ho Chung, Su Jin Yoo, Kenji Kawara, Jinhyun Kim, In Seol Yoo, Chung Gyu Park, Seong Wook Kang, Won Woo Lee

Research output: Contribution to journalArticlepeer-review

20 Scopus citations

Abstract

B7-H3, a newly identified B7 family member, has functional duality as a co-stimulator and co-inhibitor that fine- Tunes T cell-mediated immune responses. Given that B7-H3 expression on human monocytes and dendritic cells is enhanced by inflammatory cytokines, its potential inmmunoregulatory role at sites of inflammation has been suggested. Further, monocytes play crucial roles in the pathophysiology of various inflammatory disorders including autoimmune diseases; however, the immunological role of B7-H3 in rheumatoid arthritis (RA) has not been defined. Thus, we aimed to investigate the possible roles of monocyte B7-H3 in the pathogenesis of RA. Synovial monocytes, but not peripheral monocytes, in RA patients predominantly express surface B7-H3. The 4Ig isoform of B7-H3 is exclusively induced on the cell surface, whereas the 2Ig B7-H3 isoform is constitutively expressed in the intracytoplasmic region of both peripheral and synovial monocytes. B7-H3 knockdown experiments reveal that surface B7-H3 has an inhibitory effect on IFN- production in CD4 memory cells. Moreover, surface B7-H3 expression on synovial monocytes inversely correlates with RA clinical parameters. Our findings demonstrate that activation-induced B7-H3 expression on synovial monocytes has the potential to inhibit Th1-mediated immune responses and immunomodulatory roles affecting RA pathogenesis.

Original languageEnglish
Pages (from-to)4048-4057
Number of pages10
JournalJournal of Biological Chemistry
Volume291
Issue number8
DOIs
StatePublished - 19 Feb 2016

Bibliographical note

Publisher Copyright:
© 2016 by The American Society for Biochemistry and Molecular Biology, Inc.

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