The death of King Charles XII--the forensic verdict.

King Charles XII of Sweden was killed in 1718 during his siege of the Danish fortress of Fredriksten. For 276 years, it remained an open question whether the lethal bullet came from the enemy or from a Swedish assassin. Now, a treatise published by a Swedish historian finally proves that the King's death was a case of political murder.

Down-regulation of a spontaneous arthritis in male DBA/1 mice after administration of monoclonal anti-idiotypic antibodies to a cross-reactive idiotope on anti-collagen antibodies.

We recently described a spontaneously occurring, inflammatory and erosive joint disease in male DBA/1 mice. A major question is whether specific immune reactions are involved in eliciting this disease. The possibility that collagen autoimmunity might constitute one pathogenic factor was particularly interesting as this spontaneous arthritis appears to be genetically restricted in a way similar to collagen-induced arthritis.

Characterization of a spontaneously occurring arthritis in male DBA/1 mice.

Objective: We studied the incidence, severity, histopathologic features, and status of infection in a spontaneous polyarthritis which occurs in male DBA/1 mice.

Methods: Over a 25-week period, the arthritis was evaluated macroscopically in naive mice of different strains. The histopathology was evaluated at different phases of the disease.

A monoclonal antiidiotypic antibody with rheumatoid factor activity defines a cross-reactive idiotope on murine anticollagen antibodies.

A syngeneic antiidiotypic mAb, C1C3, was characterized as to its binding to monoclonal anti-collagen II (-CII) auto-antibodies reactive with different epitopes of the native CII molecule. Both by direct binding and by inhibition ELISA studies, the anti-idiotypic antibody was shown to react with a cross-reactive idiotope present on Fab fragments of most, but not all, tested anti-CII mAb, whereas the binding to Fab fragments from normal mouse IgG was low. As previously described, C1C3 bound to isolated Fc fragments from normal mouse IgG.

Down-regulation of collagen arthritis after in vivo treatment with a syngeneic monoclonal anti-idiotypic antibody to a cross-reactive idiotope on collagen II auto-antibodies.

Monoclonal anti-idiotypic antibodies previously shown to react with a cross-reactive idiotope of anti-collagen II auto-antibodies were used for in vivo treatment of DBA/1 mice receiving immunization with arthritogenic native rat collagen type II. Injection of 100 micrograms of the anti-idiotypic antibody 3 weeks before the collagen immunization resulted in a significant suppression of collagen arthritis, compared with mice treated with a monoclonal control antibody. The treatment with anti-idiotypic antibody 3 weeks before collagen immunization could also cause a marked down-regulation of the total serum levels of anti-collagen II antibodies.

Collagen induced arthritis: an experimental model for rheumatoid arthritis with involvement of both DTH and immune complex mediated mechanisms.

The type II collagen induced arthritis animal model (CIA) provides opportunities to study the nature of autoimmune reactions leading to arthritis and is also a useful model for rheumatoid arthritis (RA). Thus, in similarity with RA, the CIA when induced with autologous type II collagen, shows a chronic and progressive disease course. The susceptibility to both RA and CIA are correlated to the expression of certain MHC class II allotype genes.

Interactions between the immune system and connective tissue in arthritis. Possible significance of an affinity between IgG and native type II collagen.

The synovial inflammation in rheumatoid arthritis (RA) resembles inflammatory reactions in other tissues concerning features such as increased expression of MHC class II antigens and infiltration of large amounts of activated T lymphocytes. The present communication is concerned with how to explain features such as local production of rheumatoid factors that distinguish the synovial inflammation in seropositive RA from other chronic inflammatory reactions; We show here that monomeric IgG and, to an even higher extent, aggregated IgG show a high binding capacity for native collagen type II. This finding is discussed in the light of previous findings that native collagen II structures are readily exposed to the environment in the cartilage of inflamed joints, and the evidence that T-cell reactivity to cartilage-derived molecules among them collagen II appears to be a common feature in seropositive RA.

Generation of monoclonal rheumatoid factors after immunization with collagen II-anti-collagen II immune complexes. An anti-idiotypic antibody to anti-collagen II is also a rheumatoid factor.

Two monoclonal IgG rheumatoid factors were obtained after hybridization of spleen cells from DBA/1 mice immunized with immune complexes containing native collagen type II and a monoclonal anti-collagen II antibody. One of these rheumatoid factors reacted not only with purified murine Fc fragments, but also with Fab fragments of the anti-collagen II antibody used for immunization, whereas no reactivity was seen with Fab fragments from normal mouse IgG. The findings demonstrate the ability of immune complexes encompassing native collagen type II to induce production of IgG rheumatoid factors, and suggest that an idiotypic relationship may exist between certain rheumatoid factors and anti-collagen II antibodies.

Hyperfine structure of the 5p(5)(2)P(3/2) 5d[7/2]( degrees )(4), (2)P(3/2) 5d[3/2]( degrees )(2), and (2)P(3/2) 6p[5/2](3) levels in Cs II measured with beam-laser technique.

The hyperfine structures of the 5p(5)(2)P(3/2) 5d[7/2]( degrees )(4), (2)P(3/2) 5d[3/2]( degrees )(2), and (2)P(3/2) 6p[5/2](3) levels in Cs II have been determined in a laser-ion-beam experiment. The hyperfine-structure constants A and B for the levels have been evaluated.