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Pristane-Induced Arthritis in Mice: Genetic Regulation and Immunity in an Experimental Model of Arthritis

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H-2 Antigens

Part of the book series: NATO ASI Series ((NSSA,volume 144))

Abstract

Intraperitoneal injection of 0.5 ml of pristane (2,6,10,14-tetramethylpentadecane) caused an inflammatory arthritis in certain strains of mice. This arthritis developed in 80% – 100% of BALB/c and DBA/1 mice, but not in DBA/2, B10.RIII, B10.BR, or SWR mice, indicating regulation of susceptibility by both MHC and non-MHC genes. The BALB/c substrains also differed in their susceptibility, with the mice susceptible to ascites formation being less susceptible to arthritis and vice versa. The onset of arthritis was characterized by edema and erythema in one or more peripheral limbs. The arthritic condition persisted for over ten weeks. Several mice developed remissions and recrudescences during the course of the disease. In the majority of animals, joint deformation resulted; however, ankylosis was not detectable. Histological evaluation of the lesions showed synovial hypertrophy and pannus formation, although articular cartilage was not eroded. Periosteitis and erosions of subchondral bone were a frequent finding. Time of onset differed between strains, with DBA/1 mice developing disease 65 – 193 days after injection, and BALB/c mice, 129 – 302 days after injection. Antibodies to type II collagen were detected in sera from 75% of the arthritic mice, whereas no anti-type II antibodies developed in resistant strains. IgM RF was also detected in sera from mice immunized with pristane. Pristane-induced arthritis may represent a new model of RA.

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References

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© 1987 Springer Science+Business Media New York

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Chapdelaine, J.M., Whalen, J.D., Seibold, J.R., Wooley, P.H. (1987). Pristane-Induced Arthritis in Mice: Genetic Regulation and Immunity in an Experimental Model of Arthritis. In: David, C.S. (eds) H-2 Antigens. NATO ASI Series, vol 144. Springer, Boston, MA. https://doi.org/10.1007/978-1-4757-0764-9_75

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  • DOI: https://doi.org/10.1007/978-1-4757-0764-9_75

  • Publisher Name: Springer, Boston, MA

  • Print ISBN: 978-1-4757-0766-3

  • Online ISBN: 978-1-4757-0764-9

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