Studies on Type II Collagen Induced Polyarthritis in Rats. Effect of Complement Depletion

Kerwar, S.S.; Bauman, Norman; Oronsky, Arnold L.; Sloboda, Adolph E.

doi:10.3109/08923978109031065

Cited by 30 publications

(15 citation statements)

References 18 publications

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“…Rheumatoid arthritis Kerwar et al (1981), Linton and Morgan (1999), Wang et al (1995) Lupus erythematosus Buyon et al (1992) Myasthenia gravis Lennon et al (1978) Hyperacute rejection after xenotransplantation Dalmasso (1992), Leventhal et al (1993) Age-related macular degeneration (AMD) Edwards et al (2005), Hageman et al (2005), Haines et al (2005) Ischemia/reperfusion injury Arumugam et al (2004), Gorsuch et al (2012), Riedemann and Ward (2003) Paroxysmal nocturnal hemoglobinuria (PNH) Nishimura et al (2001), Parker et al (1985) Bullous pemphigoid Jordon et al (1973) Asthma Arroyave et al (1977) Anti-phospholipid syndrome Holers et al (2002) Atypical hemolytic uremic syndrome (aHUS) Kavanagh et al (2008) further complement activation by inactivating C3b (Banda et al, 2009). These approaches have shown encouraging results in multiple disease models with complement pathogenesis (Ricklin and Lambris, 2013).…”

Section: Disease Referencementioning

confidence: 99%

Humanized cobra venom factor: Structure, activity, and therapeutic efficacy in preclinical disease models

Vogel

Finnegan²,

Fritzinger

2014

Molecular Immunology

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Section: Disease Referencementioning

confidence: 99%

Humanized cobra venom factor: Structure, activity, and therapeutic efficacy in preclinical disease models

Vogel

Finnegan²,

Fritzinger

2014

Molecular Immunology

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“…With CIA, the disease does not regress as early or affect as many organs as extensively as AIA. Features of human RA present in CIA, but not in AIA include circulating cartilage oligomeric matrix protein and auto-immunity to cartilage driven by the presence of B-cells and auto-antibodies (2,4,14,20,22–25). Although CIA maintains a greater TH2-cell response than AIA, it is generally recognized that joint inflammation is TH1-cell driven and that these cells are the primary driving force of joint erosion and edema in CIA, AIA, and human RA.…”

Section: Introductionmentioning

confidence: 99%

Quantitative Dynamic Models of Arthritis Progression in the Rat

et al. 2008

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Purpose This comparison employs mathematical disease progression models to identify a rat model of arthritis with the least inter-animal variability and features lending to better study designs. Methods Arthritis was induced with either collagen (CIA) or mycobacterium (AIA) in either Lewis or Dark Agouti (DA) rats. Disease progression was monitored by paw edema and body weight. Models with production, loss, and feedback components were constructed and population analysis using NONMEM software was employed to identify inter-animal variability in the various disease progression parameters. Results Onset time was the only parameter different within all four groups (DA–AIA 11.5 days, DA–CIA 16.5 days, Lewis–AIA 11.9 days, Lewis–CIA 13.9 days). The loss-of-edema rate constant was 20% slower in DA (0.362 h−1) than Lewis (0.466 h−1) rats. Most models exhibited peak paw edema 20 days post-induction. Edema in CIA returned to 150% of the initial value after the disease peaked. DA rats displayed more severe overall responses. Conclusions No statistical differences between groups were observed for inter-animal variation in disease onset, progression and severity parameters. Onset time varies and should be noted in the design of future studies. DA rats may offer a more dynamic range of edema response than Lewis rats.

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“…Complement plays an important role in arthritic inflammation, as demonstrated in animal models decomplemented with cobra venom factor, where the disease appears in correlation with increasing complement levels (27). C3 particularly contributes to the local joint inflammation in CIA, as evident by the accumulation of C3 and IgG on articular cartilage (22) and the reduction of clinical scores in C3-deficient mice.…”

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confidence: 99%

Enhanced susceptibility to low‐dose collagen‐induced arthritis in CR1/2‐deficient female mice—possible role of estrogen on CR1 expression

Nilsson¹,

Andrén²,

Ståhl³

et al. 2009

FASEB j.

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The influence of complement receptor 1 and 2 (CR1/2) was investigated on the susceptibility to low-dose collagen-induced arthritis (CIA) in wild-type (WT) and CR1/2-deficient DBA/1 mice. Significantly enhanced CIA was observed in female CR1/2-deficient mice compared with WT female mice, while male mutant and WT mice showed similar arthritis development. The enhanced CIA was accompanied with higher complement levels and a prolonged IgM anti-collagen type II response. When investigating whether estrogen contributed to the different arthritis susceptibility, we found that ovariectomy rendered WT females more sensitive to low-dose CIA and to the same extent as CR1/2-deficient females, while CR1/2-deficient mice were unaffected by ovariectomy. Notably, the ovariectomized WT mice displayed reduced CR1(+) B220(+) B-cell numbers and CR1 expression compared with sham-operated WT mice, suggesting a stimulatory effect of estrogen on CR1. In accordance, a significant correlation was observed between reduced CR1 expression in B cells and increased age in healthy female blood donors but not in male donors. Our findings demonstrate an important role of CR1/2 in suppressing CIA in female mice under low-antigen conditions. The data suggest that estrogen promote CR1 expression in B cells. These findings provide insight to the increased frequency of rheumatoid arthritis in postmenopausal women.

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Studies on Type II Collagen Induced Polyarthritis in Rats. Effect of Complement Depletion

Cited by 30 publications

References 18 publications

Humanized cobra venom factor: Structure, activity, and therapeutic efficacy in preclinical disease models

Humanized cobra venom factor: Structure, activity, and therapeutic efficacy in preclinical disease models

Quantitative Dynamic Models of Arthritis Progression in the Rat

Enhanced susceptibility to low‐dose collagen‐induced arthritis in CR1/2‐deficient female mice—possible role of estrogen on CR1 expression

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