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Subclass restriction of anti-Sm antibodies in MRL mice
The subclass distribution of anti-Sm antibodies in the serum of MRL/Mp-Ipr/Ipr and MRL/Mp- +/+ mice was investigated with a sensitive ELISA technique. In both strains, but particularly in the Ipr mice, anti-Sm antibodies were predominantly of the IgG2a isotype. This preponderance was not an artifact of the sensitivity or specificity of the subclass-specific anti-Sm ELISA, nor did it reflect the subclass distribution of total serum IgG. A plaque-forming cell assay for anti-Sm antibodies also showed a predominance of the IgG2a isotype, indicating that the serum findings could not be explained by differential catabolism of IgG subclasses. Finally, antibodies to double-stranded DNA, as detected by the Crithidia luciliae assay, did not show a restricted subclass distribution. The isotype expression of anti-Sm antibodies in MRL mice must reflect in vivo mechanisms regulating the production of these autoantibodies. The IgG2a restriction in particular suggests an important in vivo role for T cells.
The subclass distribution of anti-Sm antibodies in the serum of MRL/Mp-Ipr/Ipr and MRL/Mp- +/+ mice was investigated with a sensitive ELISA technique. In both strains, but particularly in the Ipr mice, anti-Sm antibodies were predominantly of the IgG2a isotype. This preponderance was not an artifact of the sensitivity or specificity of the subclass-specific anti-Sm ELISA, nor did it reflect the subclass distribution of total serum IgG. A plaque-forming cell assay for anti-Sm antibodies also showed a predominance of the IgG2a isotype, indicating that the serum findings could not be explained by differential catabolism of IgG subclasses. Finally, antibodies to double-stranded DNA, as detected by the Crithidia luciliae assay, did not show a restricted subclass distribution. The isotype expression of anti-Sm antibodies in MRL mice must reflect in vivo mechanisms regulating the production of these autoantibodies. The IgG2a restriction in particular suggests an important in vivo role for T cells.