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These studies showed that the vast majority of CD5+ B cells, across all ages, express unmutated IgV genes, thus mirroring the situation in the mouse. The actual IgV gene repertoire of human CD5+ B cells, on the other hand, does not differ from that of CD5− B cells (Brezinschek et al. 1997). When it turned out that B-CLL can also express mutated IgV genes, models that invoked CD5+ B cells as the precursors of B-CLL had to make the assumption that IgV-mutated B-CLL are derived from CD5+ B cells that in rare instances proliferate and mutate their IgV genes in the GC reaction (Fischer et al.

2001; Dürig et al. 2003; Jelinek et al. 2003; Wang et al. 2004). The surprising theme that surfaced in these analyses was that all B-CLL cases displayed a common gene expression profile that 34 U. Klein · R. Dalla-Favera is independent of the level of IgV gene somatic hypermutation (Klein et al. 2001; Rosenwald et al. 2001) or the expression of CD38 (Dürig et al. 2003). This finding implies that B-CLL represents a homogeneous disease despite genotypic (IgV gene mutational status and genomic alterations) and clinical differences.

Cell 77:133–143 14. Kretschmer K, Jungebloud A, Stopkowicz J, Stoermann B, Hoffmann R, Weiss S (2003) Antibody repertoire and gene expression profile: implications for different developmental and functional traits of splenic and peritoneal B-1 lymphocytes. J Immunol 171:1192–1201 15. Li C, WH Wong (2001) Model-based analysis of oligonucleotide arrays: expression index computation and outlier detection. Proc Natl Acad Sci U S A 98:31–36 16. Lockhart DJ, Dong H, Byrne MC, Follettie MT, Gallo MV, Chee MS, Mittmann M, Wang C, Kobayashi M, Horton H, Brown EL (1996) Expression monitoring by hybridization to high-density oligonucleotide arrays.

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