B-1 Cell Development: Evidence for an Uncommitted Immunoglobulin (Ig)M+ B Cell Precursor in B-1 Cell Differentiation

doi:10.1084/jem.187.8.1325

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J. Exp. Med., Volume 187, Number 8, April 20, 1998 1325-1334

B-1 Cell Development: Evidence for an Uncommitted Immunoglobulin (Ig)M⁺ B Cell Precursor in B-1 Cell Differentiation

By Stephen H. Clarke and Larry W. Arnold

From the Department of Microbiology and Immunology, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina 27599

Murine phosphatidyl choline (PtC)-specific B cells in normal mice belong exclusively to the B-1 subset. Analysis of anti-PtC(V_H12 and V_H12/V $kappa$ 4) transgenic (Tg) mice indicates that exclusionfrom B-0 (also known as B-2) occurs after immunoglobulin generearrangement. This predicts that PtC-specific B-0 cells are generated,but subsequently eliminated by either apoptosis or differentiationto B-1. To investigate the mechanism of exclusion, PtC-specificB cell differentiation was examined in mice expressing the X-linkedimmunodeficiency (xid) mutation. xid mice lack functional Bruton'styrosine kinase (Btk), a component of the B cell receptor signaltransduction pathway, and are deficient in B-1 cell development.We find in C57BL/ 6.xid mice that V_H12 pre-BII cell selectionis normal and that PtC-specific B cells undergo modest clonalexpansion. However, the majority of splenic PtC-specific B cellsin anti-PtC Tg/xid mice are B-0, rather than B-1 as in their non-xidcounterparts. These data indicate that PtC-specific B-0 cell generationprecedes segregation as predicted, and that Btk function is requiredfor efficient segregation to B-1. Since xid mice exhibit defectiveB cell differentiation, not programmed cell death, these dataare most consistent with an inability of PtC-specific B-0 cellsto convert to B-1 and a single B cell lineage.

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