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Department of Microbiology and Immunology, University of North Carolina, Chapel Hill, NC 27599
The origin of B-1 cells is controversial. The initial paradigm
posited that B-1 and B-2 cells derive from separate lineages. More
recently it has been argued that B-1 cells derive from conventional B
cells as a result of T-independent Ag activation. To understand B-1
cell differentiation, we have generated Ig transgenic (Tg) mice using
the H and L chain genes (VH12 and V
4) of
anti-phosphatidyl choline (anti-PtC) B cells. In normal mice
anti-PtC B cells segregate to B-1. Segregation is intact in
VH12 (6-1) and VH12/V4 (double)
Tg mice that develop large numbers of PtC-specific B cells. However, if
B-1 cell differentiation is blocked, anti-PtC B cells in these Tg
mice are B-2-like in phenotype, suggesting the existence of an
Ag-driven differentiative pathway from B-2 to B-1. In this study, we
show that double Tg mice have a population of anti-PtC B cells that
have the phenotypic characteristics of both B-2 and B-1 cells and that
have the potential to differentiate to B-1 (B-1a and B-1b). Cyclosporin
A blocks this differentiation and induces a more B-2-like phenotype in
these cells. These findings indicate that these cells are intermediate
between B-2 and B-1, further evidence of a B-2 to B-1 differentiative
pathway.
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