scholarly journals Serum transfer of collagen-induced arthritis in mice.

1983 ◽  
Vol 158 (2) ◽  
pp. 378-392 ◽  
Author(s):  
J M Stuart ◽  
F J Dixon
Keyword(s):  
Articular Surface ◽  
Type Ii Collagen ◽  
Host Factors ◽  
Early Disease ◽  
Collagen Induced Arthritis ◽  
Serum Transfer ◽  
Immunofluorescence Studies ◽  
Resistant Strains ◽  
Arthritic Joints ◽  
Anticollagen Antibodies

Immunization of DBA/1 mice with native chick type II collagen resulted in development of polyarthritis 4-5 wk later. Sera of these mice contained high levels of anticollagen antibodies, and immunoglobulin concentrates of their sera transferred arthritis to unimmunized recipients. Histopathologically, this passively transferred arthritis resembled the early disease of immunized donors. Immunofluorescence studies demonstrated the deposition of IgG and C3 on the articular surface but not in synovial tissue of arthritic joints. Transferred, isotopically labeled anticollagen antibodies rapidly localized to the limbs and to other cartilage-containing tissues. When transfer concentrate was administered to arthritis-resistant strains, they also developed arthritis. Indeed, immunoglobulin concentrates from rats with collagen-induced arthritis transferred arthritis to naive mice. The amount of concentrate required for transfer to B10.D2 resistant mice was reduced by immunizing them with collagen 4 wk before transfer. Although susceptibility to arthritis from immunization is H-2 linked, these studies clearly demonstrate that passive transfer of arthritis depends upon injection of specific antibody and not on other host factors.

scholarly journals Type II collagen-induced arthritis in rats. Passive transfer with serum and evidence that IgG anticollagen antibodies can cause arthritis.

1982 ◽  
Vol 155 (1) ◽  
pp. 1-16 ◽  
Author(s):  
J M Stuart ◽  
M A Cremer ◽  
A S Townes ◽  
A H Kang
Keyword(s):  
Type Ii Collagen ◽  
Passive Transfer ◽  
Type Ii ◽  
Autoimmune Process ◽  
Collagen Induced Arthritis ◽  
Collagen Antibodies ◽  
Circulating Immune Complex ◽  
Early Lesion ◽  
Anticollagen Antibodies ◽  
Bovine Type

We have found that serum from rats with type II collagen-induced arthritis, when fractionated with 50% ammonium sulfate and concentrated, would transfer arthritis to nonimmunized recipients. The arthritis in recipients developed within 18-72 h and displayed all of the major histopathologic characteristics of the early lesion in immunized animals but was transient and less severe. Although consideration was given to the possibility that a circulating immune complex was involved, no evidence of such a complex was detected. Further fractionation of the serum yielded an IgG anticollagen antibody that was fully active in transferring disease. The antibody's reaction was inhibited by the native bovine type II collagen used for immunization of donors and the antibody strongly cross-reacted with homologous type II collage but not with denatured collagen. These studies demonstrate that arthritis in rats can be induced with anti-type II collagen antibodies and suggest that an autoimmune process is involved. Because antibodies to collagen have also been detected in human rheumatic diseases, further investigation of the characteristics of collagen antibodies capable of inducing arthritis seems warranted.

Effect of a novel anti-rheumatic drug, TA-383, on type II collagen-induced arthritis

1995 ◽  
Vol 17 (7) ◽  
pp. 597-603 ◽  
Author(s):  
Makoto Ueno ◽  
Kazunori Imaizumi ◽  
Takahisa Sugita ◽  
Isao Takata ◽  
Masakazu Takeshita
Keyword(s):  
Type Ii Collagen ◽  
Type Ii ◽  
Collagen Induced Arthritis ◽  
Rheumatic Drug

Evaluation of inflammatory change and bone erosion using a murine type II collagen-induced arthritis model

2010 ◽  
Vol 31 (5) ◽  
pp. 595-603 ◽  
Author(s):  
Samjin Choi ◽  
Yeon-Ah Lee ◽  
Seung-Jae Hong ◽  
Gi-Ja Lee ◽  
Sung Wook Kang ◽  
...  
Keyword(s):  
Bone Erosion ◽  
Type Ii Collagen ◽  
Inflammatory Change ◽  
Type Ii ◽  
Collagen Induced Arthritis ◽  
Arthritis Model

scholarly journals Dexamethasone Preconditioning Improves the Response of Collagen-Induced Arthritis to Treatment with Short-Term Lipopolysaccharide-Stimulated Collagen-Loaded Dendritic Cells

2013 ◽  
Vol 2013 ◽  
pp. 1-7 ◽  
Author(s):  
Corina Peña ◽  
David Gárate ◽  
Juan Contreras-Levicoy ◽  
Octavio Aravena ◽  
Diego Catalán ◽  
...  
Keyword(s):  
T Cells ◽  
Dendritic Cells ◽  
Cd4 T Cells ◽  
Combined Treatment ◽  
Type Ii Collagen ◽  
Cytokine Profile ◽  
Clinical Disease ◽  
Type Ii ◽  
Collagen Induced Arthritis ◽  
Short Term

Background. Pharmacologically modulated dendritic cells (DCs) have been shown to restore tolerance in type II collagen-(CII-) induced arthritis (CIA). We examined the effect of dexamethasone (DXM) administration as a preconditioning agent, followed by an injection of lipopolysaccharide-(LPS-) stimulated and CII-loaded DCs on the CIA course.Methods. After CIA induction, mice pretreated with DXM were injected with 4-hour LPS-stimulated DCs loaded with CII (DXM/4hLPS/CII/DCs).Results. Mice injected with DXM/4hLPS/CII/DCs displayed significantly less severe clinical disease compared to animals receiving 4hLPS/CII/DCs alone or those in which only DXM was administered. Cytokine profile evaluation showed that CD4+ T cells from DXM/4hLPS/CII/DCs and 4hLPS/CII/DCs groups release higher IL-10 levels than those from mice receiving DXM alone or CIA mice. CD4+ T cells from all DC-treated groups showed less IL-17 release when compared to the CIA group. On the contrary, CD4+ T cells from DXM/4hLPS/CII/DCs and 4hLPS/CII/DCs groups released higher IFN-γlevels than those from CIA group.Conclusion. A combined treatment, including DXM preconditioning followed by an inoculation of short-term LPS-stimulated CII-loaded DCs, provides an improved strategy for attenuating CIA severity. Our results suggest that this benefit is driven by a modulation in the cytokine profile secreted by CD4+ T cells.

scholarly journals Berberine Delays Onset of Collagen-Induced Arthritis through T Cell Suppression

2021 ◽  
Vol 22 (7) ◽  
pp. 3522
Author(s):  
Alexandra A. Vita ◽  
Hend Aljobaily ◽  
David O. Lyons ◽  
Nicholas A. Pullen
Keyword(s):  
T Cell ◽  
Type Ii Collagen ◽  
Control Group ◽  
Collagen Induced Arthritis ◽  
Preclinical Phase ◽  
T Cell Suppression ◽  
Cell Suppression ◽  
Freund’S Adjuvant ◽  
Freund's Adjuvant

There is evidence that berberine (BBR), a clinically relevant plant compound, ameliorates clinically apparent collagen-induced arthritis (CIA) in vivo. However, to date, there are no studies involving the use of BBR which explore its prophylactic potential in this model of rheumatoid arthritis (RA). The aim of this study was to determine if prophylactic BBR use during the preclinical phase of collagen-induced arthritis would delay arthritic symptom onset, and to characterize the cellular mechanism underlying such an effect. DBA/1J mice were injected with an emulsion of bovine type II collagen (CII) and complete Freund’s adjuvant (day 0) and a booster injection of CII in incomplete Freund’s adjuvant (day 18) to induce arthritis. Mice were then given i.p. injections of 1 mg/kg/day of BBR or PBS (vehicle with 0.01% DMSO) from days 0 to 28, were left untreated (CIA control), or were in a non-arthritic control group (n = 15 per group). Incidence of arthritis in BBR-treated mice was 50%, compared to 90% in both the CIA and PBS controls. Populations of B and T cells from the spleens and draining lymph nodes of mice were examined on day 14 (n = 5 per group) and day 28 (n = 10 per group). BBR-treated mice had significantly reduced populations of CD4+Th and CD4+CXCR5+ Tfh cells, and an increased proportion of Foxp3+ Treg at days 14 and 28, as well as reduced expression of co-stimulatory molecules CD28 and CD154 at both endpoints. The effect seen on T cell populations and co-stimulatory molecule expression in BBR-treated mice was not mirrored in CD19+ B cells. Additionally, BBR-treated mice experienced reduced anti-CII IgG2a and anti-CII total IgG serum concentrations. These results indicate a potential role for BBR as a prophylactic supplement for RA, and that its effect may be mediated specifically through T cell suppression. However, the cellular effector involved raises concern for BBR prophylactic use in the context of vaccine efficacy and other primary adaptive immune responses.

Oral Intake of Lactobacillus delbrueckii subsp. bulgaricus OLL1073R-1 Prevents Collagen-Induced Arthritis in Mice

2002 ◽  
Vol 65 (1) ◽  
pp. 153-160 ◽  
Author(s):  
HIROSHI KANO ◽  
TSUTOMU KANEKO ◽  
SHUICHI KAMINOGAWA
Keyword(s):  
Oral Intake ◽  
Type Ii Collagen ◽  
Inhibitory Effect ◽  
Lactobacillus Delbrueckii ◽  
Broth Culture ◽  
Control Group ◽  
Collagen Induced Arthritis ◽  
Beneficial Effects ◽  
Ifn Γ ◽  
Lactobacillus Delbrueckii Subsp

Oral intake of some lactic acid bacteria can have beneficial effects on the host by activating immune responses and enhancing resistance to infection by pathogens. In this study, effects of Lactobacillus sp. on the development of autoimmune disease were examined in mice with collagen-induced arthritis (CIA). CIA, a model of some types of rheumatoid arthritis (RA), can be induced in DBA/1J mice by immunizing them with bovine type II collagen (bCII). Oral intake of skimmed milk (SM) fermented with Lactobacillus delbrueckii subsp. bulgaricus OLL1073R-1 (SM/OLL1073R-1) was found to markedly inhibit the development of CIA in these mice, compared with a control group fed the control foodstuff. The inhibitory effect of SM fermented with L. delbrueckii subsp. bulgaricus OLL1102 (SM/OLL1102) or fresh SM was weaker than that of SM/OLL1073R-1. A deMan Rogosa Sharpe (MRS) broth culture of OLL1073R-1 without any major components of SM had the same inhibitory effect as SM/OLL1073R-1, suggesting that the inhibitory effect of SM/OLL1073R-1 is attributable not only to SM components but also to OLL1073R-1 cells, their metabolites, or both. We found that SM/OLL1073R-1 and SM caused reduced secretion of the cytokine IFN-γ by lymph node cells (LNCs) in response to bCII. However, SM/OLL1102 did not affect the secretion of IFN-γ. A polysaccharide fraction secreted by OLL1073R-1 also exhibited the inhibitory effects on both development of CIA and secretion of IFN-γ.

Serum transfer of collagen arthritis to cyclosporin-treated, type II collagen-tolerant rats

1985 ◽  
Vol 35 (2) ◽  
pp. 252-260 ◽  
Author(s):  
Nobuhiro Kaibara ◽  
Masahiro Morinaga ◽  
Chikafumi Arita ◽  
Takao Hotokebuchi ◽  
Kenji Takagishi
Keyword(s):  
Type Ii Collagen ◽  
Type Ii ◽  
Collagen Arthritis ◽  
Serum Transfer
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