A novel mechanism for the regulation of IFN-gamma inducible protein-10 expression in rheumatoid arthritis.

Abstract:

:Chemokines play an essential role in the progression of rheumatoid arthritis (RA). In the present study we examined the expression and regulatory mechanisms of IFN-gamma inducible protein (IP)-10 in RA synovitis. RA synovial fluid contained greater amounts of IP-10 than did synovial fluid from patients with osteoarthritis. Immunolocalization analysis indicated that IP-10 was associated mainly with infiltrating macrophage-like cells, and fibroblast-like cells in the RA synovium. The interaction of activated leukocytes with fibroblast-like synoviocytes resulted in marked increases in IP-10 expression and secretion. Moreover, induction of IP-10 was mediated via specific adhesion molecules, as indicated by the finding that both anti-integrin (CD11b and CD18) and intercellular adhesion molecule-1 antibodies significantly inhibited IP-10 induction. These results suggest that IP-10 expression within inflamed joints appears to be regulated not only by inflammatory cytokines but also by the physical interaction of activated leukocytes with fibroblast-like synoviocytes, and that IP-10 may contribute to the recruitment of specific subpopulations of T cells (Th1 type) from the bloodstream into the synovial joints.

journal_name

Arthritis Res Ther

authors

Hanaoka R,Kasama T,Muramatsu M,Yajima N,Shiozawa F,Miwa Y,Negishi M,Ide H,Miyaoka H,Uchida H,Adachi M

doi

10.1186/ar616

keywords:

subject

Has Abstract

pub_date

2003-01-01 00:00:00

pages

R74-81

issue

2

eissn

1478-6354

issn

1478-6362

journal_volume

5

pub_type

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