ISSN:0883-0185    

DOI:10.3109/08830188809044766

出版商:Taylor&Francis    

年代:1988

数据来源: Taylor

摘要:

Studies conducted in rats and mice indicate that passive arthritis can be transferred to naive recipients with anticollagen IgG. The passively transferred disease is less severe and is transient. Rats that recover from passive arthritis are resistant to a second phase of clinical disease when administered either anticollagen IgG or type II collagen. Suppressor T cells appear to be responsible for this resistance.Passive arthritis induced by anticollagen IgG is a complement dependent lesion. Deposition of IgG on the cartilage and host complement C3 and C5 activation are essential for the induction of passive disease. Inflammatory cells are necessary for the demonstration of passive arthritis; mice deficient in inflammatory cells or defective in this cell population are resistant to passive arthritis.Monoclonal antibodies reactive to type II collagen or to a renatured TCAfragment can also induce passive arthritis. The disease is subclinical and can be detected only after histological analysis of the joints.

ISSN:0883-0185    

DOI:10.3109/08830188809044767

出版商:Taylor&Francis    

年代:1988

数据来源: Taylor

摘要:

This review will mainly highlight data from selected, independent studies which collectively implicate a primary role for T cells in the pathogenesis of collagen arthritis in rats. Conferring insusceptibility to this experimental disease with the use of polyclonal, T cell specific antiserum provided direct initial evidence for this conclusion. Substantiation for the theory of a dominant T cell role in collagen arthritis was afforded by T cell line vaccination; scrutiny showed that the mechanism accounting for this protection was a specific down-regulation of the cellular response to collagen. Additional support came from experiments which showed that as few as 103type II collagen specific T line cells were capable of provoking a sustained proliferative synovitis when instilled into the knee joint cavity of syngeneic naive rats. Further analysis of this phenomenon revealed that the arthritogenic capacity of various collagen-reactive line cells correlated with their ability to release a 65-Kd, collagen-binding lymphokine. This antigen-specific lymphokine was designated arthritogenic factor, based on an arthritogenic activity in the knee joint bioassay similar to that of the cells. A functional and physicochemically identical rat arthritogenic factor has also been identified in the adjuvant model of arthritis. These data support the premise that a major effector mechanism in experimental rat arthritis is the release of arthritogenic factor by expanded clones of autoreactive T cells; they also indicate that substantive efforts should be undertaken to seek to identify arthritogenic factor-like lymphokines in patients with chronic inflammatory synovial disease. As an equally plausible alternative hypothesis, the review will close with a brief discussion of recent findings supporting the possible involvement of cartilage-binding, complement-fixing anti-type II collagen antibodies in the pathogenesis of rheumatoid arthritis.

ISSN:0883-0185    

DOI:10.3109/08830188809044768

出版商:Taylor&Francis    

年代:1988

数据来源: Taylor

摘要:

Arthritis could be passively transferred with a serum concentrate from collagen arthritic rats to nude rats and cyclosporin-treated, type II collagen-tolerant rats. These findings suggest that collagen arthritis could be inducible by humoral immunity alone in the absence of cellular immunity to type II collagen or functional T cells. In addition, passive arthritis induced by anticollagen antibody is a mild, transient disease from which the animals normally recover and the rats that have recovered from passive arthritis are resistant to develop a second phase of arthritis following a second administration of anticollagen antibody or the subsequent challenge with type II collagen. However, when a serum concentrate was transferred while cyclosporin was administered continuously, transferred arthritis in cyclosporin-treated, type II collagen-tolerant rats lasted as long as cyclosporin treatment and arthritis was significantly enhanced compared to those of naive recipients. Further, enhancement and prolongation of passively transferred arthritis in nude rats was observed. Furthermore, treatment with cyclophosphamide reversed acquired resistance to collagen arthritis subsequent to recovery from passive arthritis. These findings suggest that suppressor T cells might, at least in part, affect the clinical course of collagen arthritis and reverse acquired resistance to arthritis.

ISSN:0883-0185    

DOI:10.3109/08830188809044769

出版商:Taylor&Francis    

年代:1988

数据来源: Taylor

ISSN:0883-0185    

DOI:10.3109/08830188809044770

出版商:Taylor&Francis    

年代:1988

数据来源: Taylor

ISSN:0883-0185    

DOI:10.3109/08830188809044771

出版商:Taylor&Francis    

年代:1988

数据来源: Taylor

摘要:

The effects of in vivo modulation of murine collagen induced arthritis with monoclonal anti-CD4 antibodies, monoclonal anti-la antibodies, and gamma interferon are reviewed. We detail the mechanism of action of monoclonal anti-CD4 antibody on humoral and cell mediated immune responses and discuss the implications for designing therapeutic strategies. To further explore the induction of collagen induced arthritis, a syngeneic cell transfer system using collagen primed T lymphocytes is described. This cell transfer system provides an opportunity to study the role of CD4 positive T lymphocytes in arthritis induction during a short, defined time period.

ISSN:0883-0185    

DOI:10.3109/08830188809044772

出版商:Taylor&Francis    

年代:1988

数据来源: Taylor

摘要:

The present article summarizes a series of experiments which have been performed to describe an antigen-specific suppressor cell pathway for the suppression of the erythema and edema associated with an animal model of rheumatoid arthritis, collagen induced arthritis (CIA). Initial studies utilized the adoptive transfer of splenic cell subpopulations to establish the presence of suppressor cells in lymphoid tissues of mice which were suppressed for collagen induced arthritis. Subsequent studies generated T cell hybridomas from animals which had been suppressed for collagen induced arthritis by a single injection of a large quantity of Type II collagen. The T cell hybridomas varied in their self surface expression of glycoproteins which are associated with genetically determined functions. The suppressor T cells generated, described a regulatory suppressor cell pathway comprised of at least afferent suppressor T cells and effector suppressor T cells. The cells act in an antigen-specific fashion with regard to the suppression of collagen induced arthritis but appear to be polymorphic in their recognition of the interstitial collagens. The studies, taken together, indicate that the use of antigen specific T suppressor cells in the form of T cell hybridomas can be utilized as a form of immunotherapy in experimental arthritis.

ISSN:0883-0185    

DOI:10.3109/08830188809044773

出版商:Taylor&Francis    

年代:1988

数据来源: Taylor