title: Cutting edge commentary: two B-1 or not to be one.
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.
authors.affiliation: Department of Medicine, Boston University School of Medicine, MA 02118, USA. trothstein@medicine.bu.edu
authors.forename: Thomas L
authors.initials: TL
authors.lastname: Rothstein
mesh_terms: D000818:Animals; D016175:B-Lymphocyte Subsets / Q000276:immunology*; D018956:CD5 Antigens / Q000032:analysis; D002454:Cell Differentiation; D019070:Cell Lineage; D051379:Mice; D018448:Models, Immunological; D011947:Receptors, Antigen, B-Cell / Q000276:immunology; D015398:Signal Transduction; D013234:Stem Cells / Q000276:immunology
chemical_list: D018956:CD5 Antigens; D011947:Receptors, Antigen, B-Cell