Suppression of type II collagen-induced arthritis by the intravenous administration of type II collagen or its constituent peptide α1, (II) CB10

Englert, Mary E.; Landes, M. Jane; Oronsky, Arnold L.; Kerwar, S.S.

doi:10.1016/0008-8749(84)90005-4

Cited by 23 publications

(3 citation statements)

References 28 publications

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“…Both denatured collagen and peptide fragments derived by CB digestion were effective, although slightly less potent. The finding that denatured collagen fragments were effective is similar to that of Englert et al (11), who found that partially purified CB peptides enriched for CB10-induced resistance in rats. However, in the DBA/1 mouse, the most potent and consistently suppressive fragment was CB11.…”

Section: Discussionsupporting

confidence: 85%

“…Our laboratory has previously shown ( 8) that the CB11 contained critical determinants for induction ofdisease in mice . In addition, other investigators have shown that intravenous administration of soluble CII (10), collagen-coupled spleen cells (9), and partially purified collagenous peptides (11) are capable ofsuppressing collageninduced arthritis in rats. Yet localization of critical determinants for the suppressive phenomenon remained to be determined .…”

Section: Discussionmentioning

confidence: 99%

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Identification of an immunosuppressive epitope of type II collagen that confers protection against collagen-induced arthritis.

Myers

Stuart

Seyer

et al. 1989

The Journal of Experimental Medicine

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The immune response to normal joint proteins probably plays a critical role in the joint destruction of rheumatoid arthritis (for review, see references 1 and 2). Many patients have detectable immunity to various connective tissue components (3-5), and arthritis can be induced in rodents by immunizing them either with collagen or proteoglycans isolated from cartilage (6, 7). Localizing determinants ofconnective tissue with the capacity to generate immunogenic responses may give us a better understanding of the way in which arthritis is initiated and regulated.Our laboratory has previously reported (8) that a cyanogen bromide (CB)' peptide of type II collagen (CII) (CB11) carried important epitopes for the induction of arthritis in mice . We and others (9-11) have also found that injection of CII but not type I collagen intravenously would induce resistance to arthritis in rodents. Oral feeding of native but not denatured CII prevented arthritis in mice (12). However, delineation of determinants important for resistance to arthritis had not yet been reported.The present experiments were undertaken to determine if specific regions of CII capable ofinducing resistance could be identified . CII exists in vivo as a homotrimer with a rather rigid helical conformation . We first determined that, under the conditions used, either native or denatured CII (obtained by thermal denaturation) would suppress collagen-induced arthritis. We then cleaved CII into smaller fragments, isolated the resulting peptides, and tested the major ones for suppressive activity. Finally, we generated synthetic peptides, 21-26 amino acids in length, corresponding to selected regions of CB11 and injected them into either adult or neonatal mice before immunization in order to define a suppressive epitope of CII.

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Section: Discussionsupporting

confidence: 85%

Section: Discussionmentioning

confidence: 99%

Identification of an immunosuppressive epitope of type II collagen that confers protection against collagen-induced arthritis.

Myers

Stuart

Seyer

et al. 1989

The Journal of Experimental Medicine

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“…Recent studies have noted that the immune responses to collagen as well as arthritis responses in rats with CIA can be modulated by free collagen and anti collagen antiserum [9], In addition, adminis tration of collagen-coupled spleen cells [10], native type II collagen [11], or specific con stituent CNBr peptides [12] before immuni zation with type II collagen results in the antigen-specific suppression of CIA in rats. Rats administered collagen-coupled erythro cytes have also been utilized as splenic cell donors in studies showing the adoptive transfer of antigen-specific suppression of collagen arthritis [13].…”

Section: Introductionmentioning

confidence: 99%

Down-Regulation of Murine Collagen-Induced Arthritis by a T Cell Hybridoma

Kresina

1988

Pathobiology

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T cell hybridoma cell lines were generated by somatic cell fusion of BW 5147 myeloma cells and splenic cells from mice suppressed for collagen-induced arthritis (CIA). Two cell lines were characterized for their cell surface phenotype, antigen recognition and capacity to down-regulate the erythema and edema associated with CIA. Cell line T101N was determined to portray the cell surface phenotype Lyl+2- L3T4- Thyl⁺ by a direct binding assay. Cell line T104B1 was determined to express only the Thyl + alloantigen. Panning studies, measurement of IL-2 production in vitro and the suppression of antibodies to type I and type II collagen in vivo indicate that the hybridoma cells are not isotype specific in their recognition of the polymorphic interstitial collagens. Down-regulation of the erythema and edema of CIA occurred on injection of 1 × 10⁵ T101N cells but not T104B1 cells. Histology of the tarsus region of the hind paw of CIA mice 33 days after the administration of T101N cells showed contrasting histopathology compared to that of CIA mice. The joints of CIA mice given T101N cells showed aligned articular surfaces resembling normal joint structure and only residual pannus. The data indicate that collagen-specific cloned T cell lines can modulate the gross pathology and joint architecture of joints exhibiting CIA.

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Suppression of type II collagen–induced arthritis by monoclonal antibodies

Kobayashi

Terato

Harada

et al. 1991

Arthritis & Rheumatism

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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.

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Suppression of type II collagen-induced arthritis by the intravenous administration of type II collagen or its constituent peptide α1, (II) CB10

Cited by 23 publications

References 28 publications

Identification of an immunosuppressive epitope of type II collagen that confers protection against collagen-induced arthritis.

Identification of an immunosuppressive epitope of type II collagen that confers protection against collagen-induced arthritis.

Down-Regulation of Murine Collagen-Induced Arthritis by a T Cell Hybridoma

Suppression of type II collagen–induced arthritis by monoclonal antibodies

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