Surface transgenic IgM was expressed by >95% of small resting splenic B cells but only by 50% of CD5⁺ and CD5⁻ peritoneal B cells from the μ-transgenic mouse line M54. Transgenic male M54 were crossed with female CBA/N mice carrying the Xid defect. Offspring F₁ animals carrying the transgene were analysed for the presence of transgenic and endogenous IgM expressed both in the serum as well as on the surface of splenic and peritoneal B cells. We found that the levels of serum IgM coded for by the transgene were similar in both F₁ male, which lack CD5 B cells, and female transgenic mice, which have CD5 B cells. Thus, the Xid defect does not influence the expression of the transgene at the level of naturally activated plasma cells, a finding substantiated by the fact that both male and female naturally activated splenic plasma cells express the transgene at the same frequency. F₁ hybrid mice, like transgenic C57BI/6 M54 mice, have naturally activated splenic plasma cells that overexpress endogenous IgM coded for by the V_H gene family Q52. The data Indicate that normal serum IgM is not derived from CD5⁺ B cells and that the serum IgM coded for by the μ̄transgene from M54 is produced at normal levels even in the male F₁ mouse which lacks CD5⁺ B cells.