Treatment of collagen‐induced arthritis in rats with a monoclonal antibody against the α/β T cell antigen receptor

Yoshino, Shigefumi; Cleland, Leslie G.; Mayrhofer, Graham

doi:10.1002/art.1780340814

Cited by 46 publications

(24 citation statements)

References 30 publications

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“…The high level of arthritis activity persisted thereafter, resulting in ankylosis in most of the affected joints. The same doses of H57-597 injected on days 0 and 7, in contrast, provided complete protection against CIA, as previously demonstrated in rat models (15,16). Although these unexpected results would suggest a predominant role of regulatory T cells in established CIA, it was also possible that several cytokines, such as tumor necrosis factor a (TNFa), interferon-y (IFNy), or interleukin-2 (IL-2), might have been released immediately after H57-597 injection, a phenomenon similar to that related to anti-CD3 MAb injection, which in turn caused the exacerbation of arthritis.…”

Section: Resultssupporting

confidence: 76%

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Exacerbation of Established Collagen‐Induced Arthritis in Mice Treated with An Anti—T Cell Receptor Antibody

Maeda¹,

Saikawa²,

Hotokebuchi³

et al. 1994

Arthritis & Rheumatism

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Objective. To investigate the effect of T cell depletion on established collagen-induced arthritis (CIA) in mice, using monoclonal antibodies (MAb) to T cell receptor d P (TCRdP). In addition, experiments using anti-CD3 MAb were performed for comparison.Methods. CIA was induced in male DBM1 mice by immunizing them twice with bovine type I1 collagen (CII). The arthritis score and anti-CII antibody titers were examined serially. Proportions of T cells were determined by fluorescence-activated cell sorter (FACS) analysis on spleen cells or peripheral blood cells.Results. When anti-TCRdP MAb was injected on the day of CII priming, no arthritis was detected in association with depressed anti-CII antibody titers. Unexpectedly, however, when MAb was given after arthritis was established, a rapid exacerbation of arthritis was observed, which resulted in ankylosis of most joints. Anti-CII antibody titers were not affected. The addition of anti-TCRylS MAb had no effect on the augmented

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Section: Resultssupporting

confidence: 76%

“…The anti-T cell receptor (anti-TCR) MAb, R73, which recognizes T C R d P on rat T cells, has been used exclusively in rat CIA models and shown to be effective not only at the induction phase, but also at the established phase of CIA (15,16). In contrast, a recent study by Yoshino and Cleland (17) demonstrated that this MAb had no effect on chronic CIA in rats.…”

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confidence: 99%

Exacerbation of Established Collagen‐Induced Arthritis in Mice Treated with An Anti—T Cell Receptor Antibody

Maeda¹,

Saikawa²,

Hotokebuchi³

et al. 1994

Arthritis & Rheumatism

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“…There is a preponderance of evidence implicating CD4 ϩ T cells as the central mediators of disease induction in arthritis (12). Not only does susceptibility segregate with class II MHC (MHC-II) polymorphism, administration of mAbs in mouse models against TCR␣␤, CD4, and I-A all prevent disease (13)(14)(15). Recent gene array analysis of mouse MECs revealed many gene transcripts that may not be controlled by Aire (16,17).…”

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confidence: 99%

Lymphotoxin Pathway-Directed, Autoimmune Regulator-Independent Central Tolerance to Arthritogenic Collagen

Chin

Zhu

Christiansen

et al. 2006

The Journal of Immunology

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Ectopic expression of peripherally restricted Ags by medullary thymic epithelial cells (mTECs) is associated with negative selection. Autoimmune regulator (AIRE) is considered to be the master regulator of these Ags. We show in this study that the ectopic expression of type II collagen (CII) in mTECs and the corresponding central tolerance to CII are AIRE independent but lymphotoxin dependent. The failure to properly express CII in mTECs of Lta−/− and Ltbr−/− mice leads to overt autoimmunity to CII and exquisite susceptibility to arthritis. These findings define the existence of additional pathways of ectopic peripheral Ag expression, parallel to and independent of AIRE, which may cover an extended spectrum of peripheral Ags in the thymus.

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“…Of primary importance are the class I1 molecules that are encoded within the major histocompatibility complex (RTl), and that bind collagen peptides for presentation to T cells by antigen processing cells (5). Equally important are the non-major histocompatibility complex-encoded (non-MHC-encoded), T cell antigen receptor (TCR) molecules, which dictate the strength of interaction between specific T cells and each of the multiple immunogenic peptide fragments of type 11 collagen (6).…”

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confidence: 99%

Induction of autoimmune arthritis in rats by immunization with homologous rat type II collagen is restricted to the RT1^av1 haplotype

Griffiths

Cannon

Leonard

et al. 1993

Arthritis & Rheumatism

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Objective. To test for genetic differences in susceptibility to homologous (rat) type I1 collagen-induced arthritis (RII-CIA).Methods. Nine inbred and RT1-congenic rat strains were immunized with native rat type I1 collagen and evaluated for arthritis and IgG anti-RII serum antibody titers.Results. Only RTla"' strains developed a high incidence of severe RII-CIA and high titers of IgG anti-RII serum antibody. Rats having RII-CIAresistant haplotypes, RTI".".' (which are known to develop CIA after immunization with heterologous type I1 collagen), were shown to also be susceptible to passive transfer of CIA with immune serum concentrates. Clinical expression of RII-CIA was down-regulated by non-RT1 genes of BN origin. No strong gender differences in anti-RII autoimmune responses were observed.Conclusion. Arthritogenic, autoimmune reactivity to homologous RII is under strict genetic control but occurs readily in RT1"" rats. Collagen-induced arthritis (CIA) is an experimentally induced model of chronic arthritis that hasFrom The Research Service, Salt Lake City Veteran Affairs Medical Center, and the Division of Rheumatology, University of Utah Medical School, Salt Lake City, Utah.Supported been studied in rats, mice, and primates. Joint inflammation in CIA is due to the generation of collagenreactive T cells and complement-binding, IgG anticollagen antibodies that cross-react with autologous type I1 collagen in joint cartilage (1,2). Several gene products influence the susceptibility of an individual rat to CIA (3-5). Of primary importance are the class I1 molecules that are encoded within the major histocompatibility complex (RTl), and that bind collagen peptides for presentation to T cells by antigen processing cells (5). Equally important are the non-major histocompatibility complex-encoded (non-MHC-encoded), T cell antigen receptor (TCR) molecules, which dictate the strength of interaction between specific T cells and each of the multiple immunogenic peptide fragments of type 11 collagen (6).CIA is commonly induced by immunization with heterologous, native type I1 collagen extracted from the articular cartilage of diverse species including bovine, chick, deer, porcine, and human. The minor, species-specific differences in amino acid sequence that exist among these very conserved molecules are readily detected by the rat immune system and cause an RTl-restricted variability in strain susceptibility to CIA induction by type I1 collagens of different origins (7,8).In this study we analyzed the response of several inbred and RTI-congenic rat strains to immunization with homologous rat type I1 collagen (RII). Of those tested, only one MHC haplotype, RTI"", was associated with a high degree of susceptibility to RII-CIA, although the other haplotypes that were tested are known to promote the induction of CIA by immunization with heterologous type I1 collagens. The results show that MHC-encoded genes determine the

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Treatment of collagen‐induced arthritis in rats with a monoclonal antibody against the α/β T cell antigen receptor

Cited by 46 publications

References 30 publications

Exacerbation of Established Collagen‐Induced Arthritis in Mice Treated with An Anti—T Cell Receptor Antibody

Exacerbation of Established Collagen‐Induced Arthritis in Mice Treated with An Anti—T Cell Receptor Antibody

Lymphotoxin Pathway-Directed, Autoimmune Regulator-Independent Central Tolerance to Arthritogenic Collagen

Induction of autoimmune arthritis in rats by immunization with homologous rat type II collagen is restricted to the RT1^av1 haplotype

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Treatment of collagen‐induced arthritis in rats with a monoclonal antibody against the α/β T cell antigen receptor

Cited by 46 publications

References 30 publications

Exacerbation of Established Collagen‐Induced Arthritis in Mice Treated with An Anti—T Cell Receptor Antibody

Exacerbation of Established Collagen‐Induced Arthritis in Mice Treated with An Anti—T Cell Receptor Antibody

Lymphotoxin Pathway-Directed, Autoimmune Regulator-Independent Central Tolerance to Arthritogenic Collagen

Induction of autoimmune arthritis in rats by immunization with homologous rat type II collagen is restricted to the RT1av1 haplotype

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Induction of autoimmune arthritis in rats by immunization with homologous rat type II collagen is restricted to the RT1^av1 haplotype