scholarly journals Synergy between adjuvant arthritis and collagen-induced arthritis in rats.

1985 ◽  
Vol 162 (3) ◽  
pp. 962-978 ◽  
Author(s):  
J D Taurog ◽  
S S Kerwar ◽  
R A McReynolds ◽  
G P Sandberg ◽  
S L Leary ◽  
...  
Keyword(s):  
Adjuvant Arthritis ◽  
Type Ii Collagen ◽  
Passive Transfer ◽  
Lymphoid Cells ◽  
Joint Disease ◽  
Type Ii ◽  
Spleen Cells ◽  
Con A ◽  
Collagen Induced Arthritis ◽  
Immune Effector

Adjuvant arthritis (AA) in rats is susceptible to cell-mediated passive transfer. Collagen-induced arthritis (CIA) in rats is susceptible to passive transfer with antibody to type II collagen. We report here the development of strikingly severe arthritis in Lewis rats as the result of synergy between passively transferred antibody to type II collagen from rats with CIA and concanavalin A (Con A)-stimulated lymph node or spleen cells from syngeneic rats with AA. Similar synergy was seen in rats with AA given anticollagen antibody, in rats with CIA given Con A-stimulated adjuvant spleen cells, and in rats actively immunized with CII and complete Freund's adjuvant. The synergistic process caused a very severe polyarthritis, characterized by marked swelling and erythema in all the joints of the distal extremities, with histologic and radiographic evidence of early, extensive erosion of articular cartilage. Synergy was apparent if the lymphoid cells from AA rats were given up to 1 mo after a single injection of anticollagen antibody. No synergy was seen when normal rat immunoglobulin or anti-ovalbumin antibody was substituted for anticollagen antibody, when Con A-stimulated lymphoid cells from normal rats or donors with CIA were used, or when Con A-stimulated AA lymphoid cells were irradiated before transfer. Synergy between separate immune effector mechanisms may represent a general phenomenon in the pathogenesis of inflammatory joint disease.

scholarly journals Passive Transfer by Cells of Type II Collagen-Induced Arthritis in Rats

1978 ◽  
Vol 62 (2) ◽  
pp. 359-366 ◽  
Author(s):  
David E. Trentham ◽  
Roselynn A. Dynesius ◽  
John R. David
Keyword(s):  
Type Ii Collagen ◽  
Passive Transfer ◽  
Type Ii ◽  
Collagen Induced Arthritis

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.

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