| First Author | Kerner JD | Year | 1995 |
| Journal | Immunity | Volume | 3 |
| Issue | 3 | Pages | 301-12 |
| PubMed ID | 7552995 | Mgi Jnum | J:28967 |
| Mgi Id | MGI:76504 | Doi | 10.1016/1074-7613(95)90115-9 |
| Citation | Kerner JD, et al. (1995) Impaired expansion of mouse B cell progenitors lacking Btk. Immunity 3(3):301-12 |
| abstractText | 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. |
