scholarly journals IgA rheumatoid factor synthesis by dissociated synovial cells. Characterization and relationship to IgM rheumatoid factor synthesis

1985 ◽  
Vol 28 (11) ◽  
pp. 1219-1227 ◽  
Author(s):  
William J. Koopman ◽  
Ralph E. Schrohenloher ◽  
Sylvia S. Crago ◽  
David M. Spalding ◽  
Jiri Mestecky
Keyword(s):  
Rheumatoid Factor ◽  
Synovial Cells ◽  
Igm Rheumatoid Factor

scholarly journals Estimation of the relative avidity of 19S IgM rheumatoid factor secreted by rheumatoid synovial cells for human IgG subclasses

1986 ◽  
Vol 29 (6) ◽  
pp. 722-729 ◽  
Author(s):  
Dick L. Robbins ◽  
Jeffrey Skilling ◽  
William F. Benisek ◽  
Richard Wistar
Keyword(s):  
Rheumatoid Factor ◽  
Igg Subclasses ◽  
Synovial Cells ◽  
Human Igg ◽  
Igm Rheumatoid Factor

scholarly journals A spontaneous rheumatoid arthritis-like disease in MRL/l mice.

1982 ◽  
Vol 155 (6) ◽  
pp. 1690-1701 ◽  
Author(s):  
L Hang ◽  
A N Theofilopoulos ◽  
F J Dixon
Keyword(s):  
Rheumatoid Arthritis ◽  
Rheumatoid Factor ◽  
Joint Inflammation ◽  
Close Correlation ◽  
Human Rheumatoid Arthritis ◽  
Igm Rheumatoid Factor ◽  
Joint Pathology ◽  
Old Females

MRL/l mice spontaneously develop an arthritis very similar in many respects to human rheumatoid arthritis. A detailed morphologic and serologic analysis of this disease revealed the following: (a) a 75% incidence of synovial and periarticular inflammation, very similar to human rheumatoid arthritis, in 5-6 mo-old females, (b) close associations between presence of joint inflammation and subsynovial and/or periarticular vasculitis, and (c) a close correlation between presence of circulating IgM rheumatoid factor (RF) and demonstrable synovial and/or joint pathology, i.e., 95% of mice with significant levels of IgMRF had synovitis and/or arthritis.

scholarly journals COMPLEMENT FIXATION BY A TWO-COMPONENT ANTIBODY SYSTEM: IMMUNOGLOBULIN G AND IMMUNOGLOBULIN M ANTI-GLOBULIN (RHEUMATOID FACTOR)

1970 ◽  
Vol 132 (4) ◽  
pp. 673-693 ◽  
Author(s):  
Frank R. Schmid ◽  
Ivan M. Roitt ◽  
Maria J. Rocha
Keyword(s):  
Rheumatoid Factor ◽  
Complement Fixation ◽  
Direct Interaction ◽  
Fluid Phase ◽  
Kinetic Studies ◽  
Immunoglobulin M ◽  
Inhibitory Potency ◽  
Cell Agglutination ◽  
Igm Rheumatoid Factor ◽  
Rabbit Igg

Complement-mediated lysis of sheep erythrocytes coated with optimal concentrations of rabbit IgG hemolysin was inhibited by euglobulin fractions from the sera of patients with seropositive rheumatoid arthritis. That this was due to direct interaction with the IgG coat on the red cell rather than a nonspecific reaction with complement in the fluid phase was confirmed by controls using cells coated with IgM hemolysin. The inhibitory activity was recovered in purified IgM rheumatoid factor preparations and could be absorbed out with insoluble aggregated human IgG. The inhibitory potency of the rheumatoid factors correlated well with their sheep cell agglutination titers. Inhibition was not the result of physical aggregation of the erythrocytes by rheumatoid factor. Kinetic studies were consistent with the view that rheumatoid factor displaces C1q from its binding to IgG. Paradoxically, at suboptimal sensitizing concentrations of IgG hemolysin, rheumatoid factor enhances the fixation of complement. These results can be interpreted on the basis of the blockage of complement fixation by IgG and its replacement by a relatively weak direct fixation by the IgM rheumatoid factor. Thus, the interaction of RF with IgG generates only a limited ability to fix complement which, when contrasted with the fixation at suboptimal concentrations of IgG hemolysin alone, appears as net enhancement; when this is contrasted with fixation occurring with optimal concentrations of IgG, it appears as net inhibition.

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