Spontaneous and LPS-induced secretion of IgM by cultured spleen cells of NZB and SWR mice were measured after a 4-hr pulse with 3H-leucine. Similar experiments were done with fetal liver cells of NZB, CBA, BALB/c, and C57BL/6 mice. In short-term (4-hr) cultures there was marked hypersecretion of IgM by NZB cells relative to SWR cells. This abnormality was attributed to two factors: an increased number of IgM-containing cells and an increased secretion of IgM per cell. These two factors segregated as independent phenotypes in the progeny of the crosses. Liver cells from 18- to 19-day NZB fetuses matured into IgM hypersecretors in vitro in the absence of T cells. This phemomenon was uninfluenced by addition of thymocytes to cultured fetal liver cells. By contrast with the foregoing, NZB spleen cells maintained in vitro for 5 days, with or without LPS, made as much IgM during a 4-hr pulse with 3H-leucine as identically treated SWR cells. Con A-induced suppressor cells from NZB spleen cells inhibited LPS-stimulated IgM synthesis normally. There appear to be two populations of B cells in NZB mice: abnormal, spontaneously activated hypersecretors of IgM and cells that respond normally to LPS. The former population seems to arise early in life under the influence of two or three different genetic systems and functions independently of T cells.
|Original language||English (US)|
|Number of pages||8|
|Journal||Journal of Immunology|
|State||Published - Jan 1 1979|
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