Are Ly1 B cells responsible for the IL2-hyperresponsiveness of B cells in autoimmuneprone NZB x NZW F1 mice?

Unlike splenic B cells from normal BALB/c mice, those from autoimmune-prone NZB x NZW (B/W) F1 young mice were hyperresponsive to interleukin 2 (IL2) and proliferated even in the absence of prior stimulation signals. We found that the B cell subpopulation responsible for this event belongs to that with 6B2 (B220)-dull, Ly1(CD5)-positive phenotypes. Coil cycle analysis revealed that the 6B2-dull, Ly1 B cell subpopulation contains a significant number of cells at stages of G1A and G1B, while the majority of 6B2-bright B cells belongs to GO. Therefore, it appears that most of the 6B2-dull, Ly1 B cells in young B/W F1 mice are already stimulated In vivo to the stage of early activation, so that they respond to IL2 without prior stimuli. Unlike other strains of mice, including parental NZB and NZW, the B/W F1 mice showed a rapid decrease in the proportion of Botanic Ly1 B cells, beginning at about 6 months of age. This was associated with the hyporesponsiveness to IL2 of 6B2-dull splenic B cell population In the old B/W F1 mice. This phenomenon seems to relate to further activation and differentiation, which occur in Ly1 B cells with aging.