Polyclonal rheumatoid factor

Martin, T., Blaison, G., Levallois, H., Pasquali, J.L. (1992). Molecular analysis of the VkIII-Jk junctional diversity of polyclonal rheumatoid factors during rheumatoid arthritis frequently reveals N addition. Eur. J. Immunol. 22, 1773-1779. 

A major difference between a monoclonal anti-IgG and polyclonal rheumatoid factor is that the former would be expected to recognize only one kind of antigenic determinant on the IgG molecule. Stone and... 

Although monoclonal anti-IgG appears to be monospecific, anti-IgG from different patients may have different specificities. This is shown, for example, by differences in their relative strengths of interaction with human, as compared to rabbit IgG. The ratios of the two titers vary from one anti-IgG to the next and an occasional monoclonal IgM protein reacts more strongly with rabbit than with human IgG (58). Anti-IgG from one individual reacted with human IgG only after treatment of the latter with neuraminidase to remove sialic acid (59). We have not found a report of a monoclonal IgM reactive with a Gm faetor on IgG, although there are, of course, numerous instances of polyclonal rheumatoid factors with such reactivity. 

Rheumatoid factors of the IgM and IgG classes have been shown to form immune complexes in serum or joint fluid either by self-association (K17, M4, M26, P13, Sll, W21) or by reaction with native IgG (C4, K17, M4, N5, Sll, W21, W22), and these appear to be the predominant immune complex material in rheumatoid arthritis (C4, Gl, K17, M4, M26, N5, Sll, W21, W22). The primary cause of rheumatoid factor production in rheumatoid arthritis is unknown. However, rheumatoid factors are known to be present in other diseases associated with chronic antigenic stimulation (C14, M14) and can be induced in vitro by stimulation with antigens, autologous aggregated IgG, anti-idiotype reagents, and polyclonal B cell activators such as lipopolysaccharide and Epstein-Barr virus (C4, Dll, F6, F7, Gil, 16, P10, S24). Rheumatoid factors, including IgG rheumatoid factors which form selfassociating intermediate-sized (11-19 S) complexes, play a major role in... 

Pristane (2,6,10,14-tetramethylpentadecane) is a mineral oil known to induce arthritis, also called pristane-induced arthritis, in an experimental disease model (Wooley Whalen, 1991). Pristane-induced arthritis is MHC-haplotype dependent. DBA/1 mice, but not DBA/2 mice, are susceptible. The disease is accompanied by a broad spectrum of autoantibodies (rheumatoid factor, anticollagen, antibodies to heat shock protein). Pristane-induced arthritis is clearly immune dependent, since it is not observed in nu/nu mice and irradiated mice (Wooley Whalen, 1991). CD4+ T cells and polyclonal T cell activation are involved in the disease process (Wooley et al., 1998), and disease can be prevented by CD4+ Th2 cells specific for 65-kilodalton heat shock protein (Beech et al., 1997). 

Pristane-Induced Arthritis (PIA) Model. In one strain of mice, DBA/1, injection of a mineral oil pristane (2,6,10,14-tetramethylpentadecane) into joint regions induces arthritic disease associated with a broad spectrum of autoantibody production, including rheumatoid factor, anti-collagen and antiheat shock protein antibodies, and polyclonal T cell activation (Wooley and Whalen, 1991). Later work showed the ability to modulate the disease by immunoregulatory agents, e.g., administration of IL-12 cytokine (Beech et al., 1997). However, this disease-induction model appears less frequently used, likely due to lower reproducibility between laboratories, and potential... 

Williams R C Jr, Malone C C (1992). Heteroclitic polyclonal and monoclonal anti-Gm(a) and anti-Gm(g) human rheumatoid factors react with epitopes induced in Gm(a), Gm(g-) IgG by interaction with antigen or by nonspecific aggregation. A possible mechanism for the in vivo generation of rheumatoid factors. J. Immunol. 149 1817-1824. 

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