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

Some mouse monoclonal antibodies raised against chicken type I1 collagen suppressed or delayed the onset of chicken type I1 collagen-induced arthritis in DBA/l mice. This was correlated with the suppression of anti-mouse type I1 collagen antibody responses following immunization with chicken type I1 collagen. The epitopes recognized by the suppressive antibodies were found to be present on cyanogen bromide (CB)Aigested collagen peptides CB-11 and CB-12. This was also confirmed by the finding that administration of the CB-11 or CB-12 peptide suppressed the induction of arthritis.Immunization with native chicken type I1 collagen (CII) is known to cause arthritis in animals (1-3). Collagen-induced arthritis can also be adoptively transferred by sensitized spleen cells, and can be induced by passive transfer with anti-type I1 collagen antibodies (4). Moreover, for the development of arthritis, a specific epitope of collagen is important:From the Tsukuba Research Laboratories, Esai Co., Ibaraki, Japan; the Veterans Administration Hospital Medical Center, Memphis, Tennessee; and the School of Medicine, Chiba University, Chiba, Japan.Seiichi Immunization with the cyanogen bromide (CB)-digested type I1 collagen peptide 11 (CB-11 peptide), but not with other peptides, successfully induced arthritis in DBA/l mice (5). This indicates that the CB-11 peptide, rather than other portions of collagen, has an immunogenic epitope important in the induction of arthritis in the mouse.Conversely, recent studies have demonstrated that the immune response to collagen, as well as the induction of arthritis, can be modified by free collagen or anticollagen antisera (6). Administration of collagen-coupled spleen cells, native CII, a specific CB peptide, or polyclonal anti-CII before immunization with type I1 collagen results in the suppression or delayed onset of collagen-induced arthritis (6-9). Since the suppression of arthritis can be transferred by administration of splenic T cells obtained from the suppressed donor, type I1 collagen is thought to possess epitopes important for the suppression, as well as the induction, of anti-CII responses or arthritis (10).In this study, we successfully isolated monoclonal antibodies (MAb) against collagen peptides that inhibit type I1 collagen-induced arthritis. We also demonstrated that the epitopes important for the suppression of arthritis are located on the CB-11 and CB-12 peptides. MATERIALS AND METHODSMice. Male D B N l J mice (H-2q), ages 6-10 weeks, were obtained from Jackson Laboratories (Bar Harbor, ME) BALBIc mice, ages 10-20 weeks, were obtained from Charles River Japan (Atsugi, Kanagawa, Japan). All animals were housed in a barrier system and fed standard rodent chow and water ad libitum.

Section: Discussionmentioning

confidence: 99%

Suppression of type II collagen–induced arthritis by monoclonal antibodies

Kobayashi

Terato

Harada

et al. 1991

“…Since treatment of mice with either anti-T cell receptor monoclonal antibody (mAb) or anti-CD4 mAb before immunization abrogates development of the disease and CD4ϩ T cell clones reactive with CII transfer the disease to naive mice, it is believed that class II MHCrestricted CD4ϩ T cell-mediated immune reactions against CII cause the disease. Furthermore, since levels of antibody against CII have been found to correlate with the development of arthritis (14) and transfer of the antibody against CII can induce arthritis (15), most investigators believe that both cellular and humoral immunity to CII are necessary for the full development of CIA. Since antibodies against CII are also detected in humans, this model is considered to represent some aspects of the effector phase of RA (16,17).…”

Section: Conclusion These Observations Suggest That T Cell Activatiomentioning

confidence: 99%

Suppression of autoimmune arthritis in interleukin‐1‐deficient mice in which T cell activation is impaired due to low levels of CD40 ligand and OX40 expression on T cells

Saijo

Asano

Horai

et al. 2002

“…The enzyme-linked immunosorbent assay (ELISA) procedure for assaying the antibodies was essentially the same as reported earlier (26,29). Briefly, microtiter plates were coated with type I1 collagen (10 pdml in 0.1M phosphate buffer, pH 7.6).…”

Section: Estimation Of Anti-type I1 Collagen Igg Antibodiesmentioning

confidence: 99%

“…has been transferred to naive recipients by the transfer of spleen and lymph node cells from arthritic donors (31), although the number of cells required for such transfer was enormously high and the cell type(s) responsible for the phenomenon have not been identified. The disease can also be transferred with serum concentrate from arthritic rats to unimmunized recipients (29). More recently,Stuart et a1 (32) have shown that the antibody responsible for the transfer of the disease is specific to type I1 collagen, and localizes itself in the articular surface area of the joints of the recipient animals.…”

mentioning

confidence: 99%

Collagen‐induced and adjuvant‐induced arthritis in rats

Phadke

Fouts

Parrish

1984

Immunization of Lewis rats with native type I1 collagen results in an inflammatory arthritis and increased humoral and cellular immune responses to type I1 collagen. The exposure of rats to native type I1 collagen at day 7 or 10 after immunization suppressed the incidence of arthritis and anticollagen antibody levels, although the cellular response was not affected. The exposure to denatured type I1 collagen offered partial protection, while type I collagen had no significant effect. Rats immunized with Mycobucterium tuberculosis also showed reduced arthritic response when subsequently treated with type I1 collagen. The common modalities between the 2 models and the possible role of type I1 collagen in the interference with the inflammatory arthritic events are discussed.The development of immunity to collagen in various animal species has been described in the literature (1-6). Although immune responses to collagen have been detected in rheumatoid arthritis and other autoimmune diseases in humans (7-1 I), their role in the pathogenesis of these diseases is not completely understood. There has been a renewed interest in this subject since the discovery that immunization of rats and mice of certain strains with native type I1 collagen results in high levels of cell-mediated and humoral immunity, as well as inflammatory arthritis of the joints (12-15).Adjuvant-induced arthritis in rats has been extensively studied as a model for inflammatory joint diseases (16)(17)(18)(19)(20). Some of these reports provide evidence for the immunologic nature of the disease. With an intravenous injection of viable cells from lymph nodes, spleen, or thoracic duct from adjuvant arthritic rats, the disease can be transferred to the syngeneic naive recipients (17,18,20).Trentham et al have demonstrated the cellular sensitivity and detectable levels of circulating antibodies to types I and 11 collagen in adjuvant arthritic rats, as early as 1 week after the onset of arthritis (21). Holoshitz et a1 (22) have demonstrated that a T cell line derived from adjuvant arthritic rats showed a weak proliferative response to type I1 collagen in vitro. Welles and Battisto (23,24) have reported evidence showing that immunization of rats with type I1 collagen, prior to the induction of arthritis with Mycobacterium butyricum, diminished their arthritogenic response (23). Furthermore, immunization of rats with the antibodies to type I1 collagen produced a similar suppression of adjuvant arthritis (24). Recently, Cremer et al (25) have reported that intravenous pretreatment of rats with type I1 collagen does not suppress the incidence or severity of adjuvant arthritis.In the present report, we discuss the effects of intravenous treatments of rats with collagen or Mycobacterium tuberculosis on various inflammatory and immune parameters following induction of type I1 collagen or adjuvant arthritis.