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PubMed1988

Complement-activating properties of immune complexes are suppressed by IgM rheumatoid factor and enhanced by IgG rheumatoid factor.

The effect of rheumatoid factor (RF) on complement-activating capacity of aggregated IgG was investigated. The degree of complement activation induced by the addition of specific amounts of aggregated IgG to patients' sera and normal sera was demonstrated by the inhibition of hemolytic activity (%IHA). The %IHA was significantly lower in rheumatoid arthritis (RA) sera and higher in systemic lupus erythematosus (SLE) sera, compared with normal sera. There was a negative correlation between %IHA and IgMRF/IgGRF ratio in RA and SLE sera, and RA synovial fluid. The %IHA and IgGRF were positively correlated in RA sera. The IgMRF/IgGRF ratio was significantly lower in SLE sera than in RA sera and systemic sclerosis sera, and was significantly lower in RA synovial fluid than in osteoarthritis synovial fluid. Isolated RF, consisting of mostly IgMRF class, inhibited complement-activating properties of aggregated IgG, depending on the concentration of RF. Isolated RF was further purified by the fractionation using high pressure liquid chromatography, and IgGRF and IgMRF were obtained. IgMRF significantly suppressed the complement-activating capacity of aggregated IgG, whereas IgGRF promoted it. These observations suggest that IgMRF acts protectively, while IgGRF induces inflammation. Thus, the expression of the biological activity of RF with special reference to immune complex interaction mainly depends on the IgMRF/IgGRF ratio.

Antigen-Antibody Complex↗
PubMedDate not supplied

Rheumatoid factor diversity.

Rheumatoid factors, antibodies directed against the Fc portion of IgG, exhibit considerable isotypic and idiotypic diversity. Differential expression of IgM and IgA rheumatoid factors suggests that isotype-specific regulatory pathways are operative in man. The physical characteristics of IgA rheumatoid factor in rheumatoid arthritis have also been investigated. Although the polymeric form of IgA rheumatoid factor generally predominates in sera and synovial fluids of rheumatoid arthritis patients, wide variations in the ratio of monomeric to polymeric IgA rheumatoid factor are observed. Both forms are elaborated by synovial plasma cells. That differences in the proportions of monomeric and polymeric IgA RF present in sera may be of pathogenetic significance is suggested by evidence that complexes of polymeric IgA rheumatoid factor and IgG are potent inducers of lysosomal release by RMN whereas monomeric IgA rheumatoid factor-IgG complexes are essentially inactive in this regard. The idiotypic diversity of rheumatoid factors has also been under intensive investigation. A monoclonal antibody designated 6B6.6 recognizes a Vk-associated idiotype present on approximately one-third of IgMk rheumatoid factor paraproteins, but only a small fraction of polyclonal IgM 6B6.6-defined idiotype is distinct from previously described rheumatoid factor cross-reactive idiotypes. Taken together, these studies underline the extensive diversity of rheumatoid factors present in various conditions. Application of molecular genetic approaches to the study of rheumatoid factors should provide explanations for the molecular basis of this diversity and serve to clarify the relationship among rheumatoid factors expressed in both physiologic and pathologic states.

Antibody Diversity↗
PubMed1988

Effects of piroxicam and D-penicillamine on T lymphocyte subpopulations, natural killer cells and rheumatoid factor production in rheumatoid arthritis.

The effects of piroxicam and D-penicillamine on T lymphocytes, NK cell activity and rheumatoid factor production as well as clinical parameters were studied in patients with rheumatoid arthritis. The level of total rheumatoid factor fell during treatment with D-penicillamine (p less than 0.02) and there was a positive correlation (K greater than 0.50, p less than 0.05) between this fall in rheumatoid factor and the improvement of several clinical activity parameters. No significant change was observed in the level of rheumatoid factor during treatment with piroxicam. Natural killer cell activity decreased from 21.1 +/- 2.5 to 15.8 +/- 1.9 after treatment with piroxicam for 3 weeks (p less than 0.05) as compared with changes in the controls. No change in natural killer cell activity was seen after treatment with D-penicillamine. Moreover, no significant changes in the numbers of T4+ and T8+ lymphocytes nor in the numbers of HLA-DR positive T cells were seen in the two treatment groups. Both laboratory and clinical activity parameters improved during the treatment with D-penicillamine, while only subjective parameters improved during treatment with piroxicam.

Adolescent↗