Journal
INTERNATIONAL IMMUNOLOGY
Volume 16, Issue 3, Pages 455-465Publisher
OXFORD UNIV PRESS
DOI: 10.1093/intimm/dxh045
Keywords
autoimmune disease; knock-in mouse; rheumatoid arthritis; Tax
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Rheumatoid arthritis (RA) is a polygenic autoimmune disease. The autoimmunity develops from synergistic actions of genetic and environmental factors. We generated a double-mutant mouse by crossing two murine models of RA, a gp130 mutant knock-in mouse (gp130(F759/F759)) and an HTLV-1 pX transgenic mouse (pX-Tg), in a C57BL/6 background, which is resistant to arthritis. The mice spontaneously developed severe arthritis with a much earlier onset than the gp130(F759/F759) mice and with a much higher incidence than did the pX-Tg mice. The symptoms of gp130(F759/F759) mice, including lymphoadenopathy, splenomegaly, hyper-gamma-globulinemia, autoantibody production, increases in memory/activated T cells and granulocytes in the peripheral lymphoid organs, and a decrease in the class II MHCbright CD11c(+) population, were augmented in the double mutants. Marked reductions in incidence, severity and immunological abnormalities were seen in the triple mutant, IL-6(-/-)/gp130(F759/F759)/pX-Tg, indicating that the arthritis in the double mutant is IL-6 dependent. gp130(F759/F759)/pX-Tg is a unique mouse model for RA.
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