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. 1995 Sep;3(3):301-12.
doi: 10.1016/1074-7613(95)90115-9.

Impaired expansion of mouse B cell progenitors lacking Btk

J D Kerner  1 , M W Appleby, R N Mohr, S Chien, D J Rawlings, C R Maliszewski, O N Witte, R M Perlmutter
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Free article

Impaired expansion of mouse B cell progenitors lacking Btk

J D Kerner et al. Immunity. 1995 Sep.
Free article

Abstract

Mutations in the gene encoding the protein tyrosine kinase Btk are associated with the human B cell immunodeficiency X-linked agammaglobulinemia (XLA). In the mouse, a point mutation in the Btk pleckstrin homology domain segregates with a milder X-linked immunodeficiency (xid). To assess the importance of Btk function in murine lymphopoiesis, we generated multiple embryonic stem cell clones bearing a targeted disruption of the btk gene and examined their potential to produce lymphocytes in both C57BL/6 and RAG2-/- host chimeric animals. These mice provide a complementary set of in vivo competition assays that formally establish the genetic basis for the xid phenotype. Although the null mutation yields a phenotype quite similar to that of xid, it also compromises expansion of B cell precursors. Our results suggest that the murine and human consequences of Btk deficiency differ only quantitatively, and represent the same disease process.

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