Pathogenic lymphoid cells engineered to express TGF β1 ameliorate disease in a collagen-induced arthritic model
Collagen-induced arthritis in DBA/1 mice is a model of rheumatoid arthritis with marked synovitis and erosions. The disease can be adoptively transferred to SCID mice with arthritogenic splenocytes from DBA/1 mice injected with bovine collagen type II. However, infection of arthritogenic splenocytes...
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| Autores principales: | , , , , |
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| Formato: | JOUR |
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| Acceso en línea: | http://hdl.handle.net/20.500.12110/paper_09697128_v4_n6_p553_Chernajovsky |
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| Sumario: | Collagen-induced arthritis in DBA/1 mice is a model of rheumatoid arthritis with marked synovitis and erosions. The disease can be adoptively transferred to SCID mice with arthritogenic splenocytes from DBA/1 mice injected with bovine collagen type II. However, infection of arthritogenic splenocytes with a retrovirus expressing TGF β1 inhibits development of arthritis in SCID mice. When DBA/1 mice, at onset of arthritis have additional arthritgenic splenocytes transferred, exacerbation occurs, reflected in a rapid increase in the number of arthritic joints, increased paw swelling and higher levels of anti-collagen antibody. By infecting arthritogenic splenocytes ex vivo with TGF β1 retrovirus, this exacerbation was inhibited. TGF β1 was effective in lowering inflammation of joints with already established arthritis and inhibiting the spreading of the disease to other joints. Transient reduction on anti-collagen antibody levels could also be obtained using purified T cells infected woth TGF β1 retrovirus. In addition, expression of TGF β1 in lymphocytes reduced the levels of gelatinase (MMP2) activity in inflamed joints. |
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