作者: J M Stuart , A S Townes , A H Kang
DOI: 10.1146/ANNUREV.IY.02.040184.001215
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摘要: The evidence is now fairly conclusive that collagen-induced arthritis in rodents mediated by antitype II collagen autoimmunity. Arthritis probably initiated binding of antibodies to the surface intact articular cartilage. Many major manifestations arthritis, including synovial proliferation, pannus formation, marginal erosion bone, and destruction cartilage, can be duplicated injection isolated antibodies. It not known whether delayed hypersensitivity reactions provoke similar lesions absence antibody, but circumstantial suggests they do not. Also clear all anticollagen are capable inducing arthritis. minimal requirements for arthritogenic potential currently under investigation include ability bind native autologous type collagen. IgM alone either ineffective or required relatively higher concentrations than IgG induction Autoimmunity found many spontaneous induced rheumatic diseases other There at present, however, no direct this autoimmunity actually contributes arthritic process. Nevertheless, human disease most often associated with rheumatoid In respects immune detected humans parallel those rodents. That is, responsiveness control genes within linked histocompatibility locus. High responders limited only a few haplotypes. Cell-mediated vigorous response denatured have specificity recognized. Antibodies may separated into least two groups, one broad second highly specific conformation-dependent determinants on latter interest researchers because like induce also ample deposited joints patients, although these unknown. Generally, model antibody-initiated Specifically, it autoimmune consideration its extraarticular manifestations, justifiably referred as disease.(ABSTRACT TRUNCATED AT 400 WORDS)