role of fibrinogen-like protein 2 (FGL2)/fibroleukin in the pathogenesis of experimental autoimmune arthritis.
Published: 2005
Language: eng
Number of pages: 113
Description: Fibrin deposition is a prominent feature and major contributor to the pathogenesis of RA. Fibrinogen-like protein 2 (fgl2) is an inducible prothrombinase that plays an important role in fibrin deposition during viral hepatitis and cytokine-induced fetal loss. CIA in DBA/1 mice revealed that fgl2 mRNA transcripts and protein were markedly upregulated in arthritic joints. Fibrin deposition was prominent within the synovial lining and articular joint space, in close association with fgl2 expression. Infusion of murine CD200Fc inhibited the development of CIA and expression of fgl2 mRNA transcripts and protein in DBA/1 mice. The decrease in fgl2 expression was also associated with inhibition of fibrin deposition. Development of collagen type II monoclonal antibody-induced arthritis was inhibited in fgl2-/- mice in comparison to fgl2+/+ mice, which developed a severe inflammatory arthritis with clinical and m2 histological manifestations associated with RA. These observations suggest that fgl2 contributes to fibrin deposition in RA and provides a rationale for targeting fgl2 to ameliorate RA.
Notes: Source: Masters Abstracts International, Volume: 44-02, page: 0812.

Thesis (M.Sc.)--University of Toronto, 2005.

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