Abstract
B-1 cells differ from conventional B-2 cells both phenotypically and functionally. Two seemingly mutually exclusive hypotheses have been proposed to explain the origin of B-1 cells. The lineage hypothesis holds that certain B cell precursors are destined early on to become B-1 cells. The differentiation hypothesis holds that every B cell has the same potential to acquire B-1 characteristics. Reconsideration of previous studies of transgenic and knockout mice, plus recent results identifying differences between splenic and peritoneal B-1 cells, point to unexpected complexity in the pathway leading to B-1 status. A new paradigm is suggested, in which surface Ig signaling is required for B-1 cell production, but in which the signaling threshold and context that lead to B-1 cell development and/or expansion differ for particular B cell precursors. Surface Ig signaling may also produce receptor editing, apoptotic deletion, and tolerance induction; how these different outcomes are determined remains uncertain.
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