Journal
JOURNAL OF LEUKOCYTE BIOLOGY
Volume 90, Issue 4, Pages 811-817Publisher
WILEY
DOI: 10.1189/jlb.1110640
Keywords
Flt3 ligand; inflammation
Categories
Funding
- Medical Society of Goteborg
- Swedish Association against Rheumatism
- King Gustaf V:s Foundation
- Swedish Research Council
- Professor Nanna Swartz Foundation
- AME Wolff Foundation
- Rune and Ulla Amlovs Trust
- Swedish Foundation for Strategic Research
- Soderberg's Foundation
- Pharmacist Hedberg's Foundation
- University of Goteborg
- Family Tholen and Kristlers Foundation
- European Union Commission
- Western Gotaland County Council
- University of Goteborg (LUA/ALF)
- Reumatikerdistriktet I Goteborg
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TKs are intracellular signaling molecules essential for cell homeostasis. Inhibition of TKs is used in treatment of malignancies and diabetes mellitus. The present study evaluated the role of Flt3 in antigen-induced arthritis. Mice were immunized with mBSA, and arthritis was induced by an i.a. injection of mBSA. Treatment with the Flt3 inhibitor sunitinib was started together with mBSA immunization or together with the induction of arthritis. The mBSA-injected joints were evaluated morphologically for signs of synovitis and bone/cartilage destruction. Markers of bone metabolism and antibody responses were measured by ELISA. Maturation of DCs in the bone marrow and spleen was evaluated by flow cytometry. Sunitinib treatment reduced the intensity of synovitis and the incidence of bone destruction. The reduction in bone destruction was seen when the treatment was started at the time of immunization or at the time of arthritis induction. The antiarthritic effect was achieved by inhibition of DCs, reduction of antibody production, and bone metabolism. Inhibition of Flt3 is a potent antiarthritic mechanism reducing antigen presentation, synovial inflammation, and bone resorption. Down-regulation of TKs may be a useful tool in the treatment of human RA. J. Leukoc. Biol. 90: 811-817; 2011.
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