The regulatory locus r lambda 1 affects the level of lambda 1 light chain synthesis in lipopolysaccharide-activated lymphocytes but not the frequency of lambda 1-positive B cell precursors.

Several strains of mice, most notably the SJL strain, have a greatly reduced level of circulating lambda 1 immunoglobulins (r lambda 1 lo phenotype) compared with other mice. The locus responsible for this phenotype has been shown to be closely linked to the structural C lambda 1 gene. Functionally this locus has been said to reduce the number of lymphocytes expressing surface lambda 1 molecules. In order to gain a better understanding of this phenomenon we compared the functional properties of activated B cells secreting lambda 1 immunoglobulins in the splenocytes of both BALB/c and SJL mice. Our results indicate that regulatory T cells, as well as regulatory ontogenetic processes, are not responsible for the r lambda 1 lo phenotype. In addition, limiting dilution analyses revealed that the number of lipopolysaccharide-sensitive precursors of lambda 1-secreting B cells was similar in the splenocytes of the two strains of mice tested. The quantity of lambda 1 molecules produced by a B cell clone, however, was found to be lower in SJL than in BALB/c mice. As the level of lambda 1 mRNA is greatly reduced in lipopolysaccharide blasts of SJL mice, as compared to the mRNA detected in BALB/c blasts, we conclude that the impairment responsible for the r lambda 1lo phenotype is probably transcriptional. We tentatively propose that sequences 5' to the C lambda 1 region are defective in their capacity to enhance the lambda 1 transcripts in SJL mice.