Prostaglandin E2 and collagenase release by cultured talus from type II collagen arthritis rats

1986 ◽  
Vol 19 (5-6) ◽  
pp. 320-322
Author(s):  
D. Westmacott ◽  
J. E. Hawkes ◽  
J. Wadsworth ◽  
C. H. Cashin ◽  
A. Cline ◽  
...  
Keyword(s):  
Prostaglandin E2 ◽  
Type Ii Collagen ◽  
Type Ii ◽  
Collagen Arthritis

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

Murine type II collagen arthritis: Association of an acute-phase response with clinical course

1986 ◽  
Vol 29 (9) ◽  
pp. 1131-1138 ◽  
Author(s):  
Marcia L. Bliven ◽  
Paul H. Wooley ◽  
Mark B. Pepys ◽  
Ivan G. Otterness
Keyword(s):  
Acute Phase ◽  
Acute Phase Response ◽  
Clinical Course ◽  
Type Ii Collagen ◽  
Phase Response ◽  
Type Ii ◽  
Collagen Arthritis

scholarly journals Paradoxical effects of cyclosporin A on collagen arthritis in rats.

1983 ◽  
Vol 158 (6) ◽  
pp. 2007-2015 ◽  
Author(s):  
N Kaibara ◽  
T Hotokebuchi ◽  
K Takagishi ◽  
I Katsuki
Keyword(s):  
T Cells ◽  
Cyclosporin A ◽  
Type Ii Collagen ◽  
Delayed Type Hypersensitivity ◽  
Induction Phase ◽  
Dependent Manner ◽  
Type Ii ◽  
Skin Reactions ◽  
Collagen Arthritis ◽  
Paradoxical Effects

The effect of the immunosuppressive agent cyclosporin A (CS-A) on collagen arthritis in Sprague-Dawley rats is investigated. A 14-d course of CS-A treatment at doses of 15 mg/kg per day or more, begun on the same day as type II collagen immunization, suppressed the development of arthritis as well as humoral and delayed-type hypersensitivity (DTH) skin test responses to type II collagen, possibly by interfering with helper T cells. Additional studies demonstrated that CS-A treatment only during the induction phase of immunity proved to be successful. When CS-A treatment was started only during the immediately preclinical phase of arthritis or after the disease onset, a significant enhancement of the disease was obtained in a dose-dependent manner. This enhancement was accompanied by an augmentation of DTH skin reactions, while antibody responses were either suppressed or unaffected. These results appear to be attributable at least in part to a suppressive effect of CS-A on a population of suppressor T cells, thus resulting in a T cell-mediated helper effect. It is therefore reasonable to assume that the paradoxical effects of CS-A on collagen arthritis in rats might be caused by an altering of the sensitive balance of the two regulatory subpopulations of T cells. It is also possible that cell-mediated immune responses may play an important role in influencing the course of the disease.

scholarly journals Type II collagen-induced arthritis in mice. I. Major histocompatibility complex (I region) linkage and antibody correlates.

1981 ◽  
Vol 154 (3) ◽  
pp. 688-700 ◽  
Author(s):  
P H Wooley ◽  
H S Luthra ◽  
J M Stuart ◽  
C S David
Keyword(s):  
Disease Susceptibility ◽  
Type Ii Collagen ◽  
Type Ii ◽  
Collagen Induced Arthritis ◽  
Histocompatibility Complex ◽  
Low Responders ◽  
Collagen Arthritis ◽  
Histological Appearance ◽  
Antibody Levels ◽  
F1 Cross

A model of arthritis was established by the injection of type II collagen into mice. Only mice bearing the H-2q haplotype were susceptible to the disease. Susceptibility was further mapped by the use of recombinant strains on the Iq locus. Type II collagen arthritis was observed in the (resistant X susceptible) F1 cross. Mice strains were designated high, intermediate, or low responders with respect to the anti-type II antibody levels measured by radioimmunoassay. Arthritis-susceptible strains were all classified as high antibody responders. The clinical and histological appearance of type II collagen arthritis in the mouse indicates that it may be a good animal model for the investigation of various immunogenetic traits in rheumatoid arthritis.

scholarly journals An arthritogenic lymphokine in the rat.

1985 ◽  
Vol 162 (5) ◽  
pp. 1531-1545 ◽  
Author(s):  
S M Helfgott ◽  
R Dynesius-Trentham ◽  
E Brahn ◽  
D E Trentham
Keyword(s):  
T Cells ◽  
T Cell ◽  
Knee Joint ◽  
Type Ii Collagen ◽  
Type Ii ◽  
Effector Mechanism ◽  
Collagen Arthritis

A type II collagen-specific arthritogenic lymphokine has been identified in the rat. Arthritogenic factor (AF) is a 65 kD protein generated in vitro by T cells from rats with collagen arthritis, and it induces an erosive, proliferative synovitis when injected into the knee joint of syngeneic naive recipients. Complement does not appear to be required. These data identify a potential T cell-mediated effector mechanism in this model, and suggest that AF may function in other inflammatory synovial diseases.

Assessment of drugs for activity in established type II collagen arthritis

1982 ◽  
Vol 12 (5) ◽  
pp. 650-656 ◽  
Author(s):  
S. A. Jones ◽  
A. J. Kennedy ◽  
N. A. Roberts
Keyword(s):  
Type Ii Collagen ◽  
Type Ii ◽  
Collagen Arthritis

Type II collagen arthritis: Identification of arthritogenic epitopes using fractionated anticollagen IgG

1987 ◽  
Vol 105 (2) ◽  
pp. 447-453 ◽  
Author(s):  
Mary E. Englert ◽  
Kim M. Ferguson ◽  
Carmen R. Suarez ◽  
Theresa M. Sapp ◽  
Arnold L. Oronsky ◽  
...  
Keyword(s):  
Type Ii Collagen ◽  
Type Ii ◽  
Collagen Arthritis

scholarly journals Pathogenetic difference between collagen arthritis and adjuvant arthritis.

1984 ◽  
Vol 159 (5) ◽  
pp. 1388-1396 ◽  
Author(s):  
N Kaibara ◽  
T Hotokebuchi ◽  
K Takagishi ◽  
I Katsuki ◽  
M Morinaga ◽  
...  
Keyword(s):  
Adjuvant Arthritis ◽  
Critical Role ◽  
Type Ii Collagen ◽  
Complete Suppression ◽  
Type Ii ◽  
Sprague Dawley ◽  
Cyclosporin Treatment ◽  
Collagen Arthritis ◽  
Treatment Type ◽  
Mycobacterial Cell Wall

Daily treatment with cyclosporin at a dose of 25 mg/kg for 14 d gave complete suppression of the development of collagen arthritis and adjuvant arthritis in Sprague-Dawley rats during an observation period of 45 d. To study whether the immunologic unresponsiveness produced by cyclosporin is antigen specific, we rechallenged the cyclosporin-protected rats with either type II collagen or complete Freund's adjuvant (CFA) after discontinuation of cyclosporin treatment. Type II collagen-immunized, cyclosporin-protected rats did not develop arthritis in response to reimmunization with type II collagen, but, they did develop arthritis in response to a subsequent injection of CFA. Similarly, CFA-injected, cyclosporin-protected rats showed a suppressed arthritogenic reaction in response to reinjection of CFA, whereas their response to a subsequent immunization with type II collagen was unaffected. On the other hand, the rats that were treated with cyclosporin without any prior antigenic challenge could develop arthritis in response to a subsequent injection of CFA or type II collagen after cessation of cyclosporin treatment. These results indicate that specific immunologic unresponsiveness can be induced by cyclosporin in the two experimental models of polyarthritis, collagen arthritis and adjuvant arthritis, and that there is no cross-reactivity between type II collagen and the mycobacterial cell wall components. The results further indicate that immunity to type II collagen plays a critical role in the pathogenesis of collagen arthritis but that its pathogenetic role in adjuvant arthritis is insignificant.

scholarly journals Rat cytomegalovirus infection enhances type II collagen arthritis in rats

1986 ◽  
Vol 29 (10) ◽  
pp. 1263-1268 ◽  
Author(s):  
Charles B. Smith ◽  
Marie M. Griffiths ◽  
Lian S. Wei
Keyword(s):  
Cytomegalovirus Infection ◽  
Type Ii Collagen ◽  
Type Ii ◽  
Collagen Arthritis
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