Exacerbation of Established Collagen‐Induced Arthritis in Mice Treated with An Anti—T Cell Receptor Antibody

Maeda, Takeshi; Saikawa, Isao; Hotokebuchi, Takao; Sugioka, Yôichi; Eto, Masatoshi; Murakami, Yoshiyuki; Nomoto, Kikuo

doi:10.1002/art.1780370315

Cited by 23 publications

(10 citation statements)

References 34 publications

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“…Thus, IL-10 might be a good prophylactic agent, but a poor therapeutic agent for the treatment of RA. Similar observations were recently reported in studies using anti-TCRc~//3 mAb [22] and anti-TCR,~/~ mAb [25]. Early injections of anti-TCRa/fl mAb completely prevented the development of arthritis in CII-immunized mice.…”

Section: Discussionsupporting

confidence: 89%

“…The arthritic index (AI) was assessed with reference to the controls as described [22]. One week after the second immunization, it was clear that the A!…”

Section: Resultsmentioning

confidence: 99%

“…CII was isolated and purified from bovine articular cartilage, as previously reported [22]. Each DBA/1 mouse was immunized at the base of the tail with 200 gg of native collagen in Complete Freund's adjuvant (Difco, Detroit, MI, USA), followed by booster injections at 3 weeks.…”

Section: Preparation Of Type II Collagen ( Cii) and Production Of Ciamentioning

confidence: 99%

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Effect of IL-10 on collagen-induced arthritis in mice

et al. 1996

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Abstract. In the present study we investigated the effect of a potent anti-inflammatory cytokine, interleukin (IL)-10, on the development of collagen-induced arthritis (CIA) in mice. Each DBA1/J mouse was immunized with 200 gg of native collagen and followed by booster injections at 3 weeks, rmIL-10 was injected i.p. daily at a dose of 100ng/mouse. Mice were divided into four groups according to the administration period of rmIL-10. As a result, a 48-day course of IL-10 treatment significantly suppressed the severity of arthritis. Among the 4 groups, the most pronounced suppression was observed in the group in which IL-10 was given from day 0 to 21. On the other hand, there were no significant differences in the serum IgG anti-type II collagen (CII) titers between the four groups. Moreover, the production of cytokines (IL-6 and tumor necrosis factor-oz (TNF-c~)) and other mediators (prostaglandin E2 (PGE2) and nitric oxide (NO)) by peritoneal macrophages seemed to show no clear correlation with the severity of arthritis in mice. These results raise the possibility that IL-10 might be a useful agent for suppressing the progression and the development of CIA in mice.

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Section: Discussionsupporting

confidence: 89%

“…The arthritic index (AI) was assessed with reference to the controls as described [22]. One week after the second immunization, it was clear that the A!…”

Section: Resultsmentioning

confidence: 99%

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Effect of IL-10 on collagen-induced arthritis in mice

et al. 1996

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“…Treatment of established CIA with anti-T cell receptor aj0 antibodies has been reported either to reduce disease severity [25,26] or to exacerbate disease [27]. Given that the CD5 antigen and T cell receptor/CD3 complex are physically associated in T cells [28,29], the observed reduetion in severity of established CIA following immunotherapy directed at the T ceil receptor ajj-i or CD5 antigen may conceivably be mediated via a common pathway.…”

Section: Discussionmentioning

confidence: 99%

Anti-CD5 therapy decreases severity of established disease in collagen type II-induced arthritis in DBA/1 mice

Plater-Zyberk

Taylor

Blaylock

et al. 1994

Clinical and Experimental Immunology

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SUMMARYCollagen-induced arthritis has been widely used as an animal model of rheumatoid arthritis. We have used this model with a view to determining potential therapeutic targets for the treatment of human disease. To do this we have attempted to modulale the progression of established arthritis over a 10-day time period following the first appearance of disease, by i.p. injection of one of three different MoAbs. These eonsist of a rat IgG2a specific for the CD5 antigen expressed on all T cells and a subpopulation of B eells, a mouse IgG2b recognizing the CD72 antigen, and a rat IgM speeifie for the B220 molecule, CD72 and B220 both being expressed on all B cells. None of the three MoAbs had depleting activity in vivo. The progression of arthritis was monitored both clinically, and histologically. The effects of treatment with anti-CD5 and anti-CD72 antibodies were compared with control antibodies ofthe same species class and subclass. In the case of anti-B220 antibodies, the effects of treatment were eompared with administration of FBS. Of these MoAbs, only treatment with anti-CD5 resulted in disease amelioration with significant decrease in disease severity in 60% of the animals. These changes became apparent 6 days after initiation of treatment. There were no significant differences in serum levels of IgG antibodies to native bovine collagen type II between the groups of treated and control mice. Possible meehanisms underlying the modification of disease expression following treatment with anti-CD5 MoAb are discussed.

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“…The question mark grows if we also consider recently published and emerging data which show that the TCR usage of CII-reactive T cells derived from H-2q mice is very diverse ( [42,43] and Corthay et al, submitted). It should be emphasized, however, that anti-T cell antibody treatment experiments to affect the development of CIA may give unexpected result possibly due to activation of remaining regulatory T cell subpopulations [44,45]. A role for a limited TCR usage by cells actually mediating the disease in the H-2q mice can, however, not be excluded.…”

Section: Collagen Type H Arthritismentioning

confidence: 99%