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We next assessed if these long-lived t(14;18)-bearing B cells in HI already transited through the GCs. Circulating naive and memory B cells can be distinguished on the basis of the CD27 cell surface marker and sIg isotypes (11–13). Fresh PBMCs from 10 healthy donors were collected, and IgD⁺/CD27^– naive, IgD⁺/CD27⁺ memory, and IgD^–/CD27⁺ switched memory B cell subsets isolated by cell sorting (Fig. 2 A). The occurrence of t(14;18) was then assessed in total PBMCs and in each fraction by the short-range BCL2/J_H PCR assay (Fig. 2 B and Table II). As a first approach, we pooled data from the two CD27⁺ memory subsets and examined the overall contribution of naive (CD27^–) and memory (CD27⁺) B cells to the total t(14;18)⁺ frequency calculated as a fraction of CD19⁺ B cells (Fig. 2 C). t(14;18) frequencies of CD19⁺ B cells ranged from <1/10⁵ to the unexpectedly high rate of 1/3.500 B cells in some individuals (Fig. 2 C, squares). Strikingly, although the level of naive t(14;18)⁺ cells constantly remained at baseline (Fig. 2 C, circles), CD27⁺ B cells accounted in a large part for the amplitude of t(14;18) frequencies (Fig. 2 C, triangles). This clearly indicates that circulating t(14;18)⁺ clones in HI are indeed predominantly B cells which transited through the GCs. To determine if the presence of high levels of t(14;18) in some individuals was caused by a higher incidence of distinct translocations or to the clonal expansion of a given t(14;18)⁺ B cell, we cloned and sequenced 55 out of 61 BCL2/J_H fragments from the CD27⁺ subset. One major BCL2/J_H junction was observed in most individuals (Fig. 2 D, black bars), indicating that only one clone mainly accounted for t(14;18) frequencies. Remarkably, this data demonstrate that the wide modulation of t(14;18) frequency in HI is not caused by the accumulation of clonally unrelated t(14;18) naive B cells in some individuals, but rather to the clonal expansion in the GCs of t(14;18)⁺ B cells.