| First Author | Ellmeier W | Year | 2000 |
| Journal | J Exp Med | Volume | 192 |
| Issue | 11 | Pages | 1611-24 |
| PubMed ID | 11104803 | Mgi Jnum | J:66080 |
| Mgi Id | MGI:1927949 | Doi | 10.1084/jem.192.11.1611 |
| Citation | Ellmeier W, et al. (2000) Severe B cell deficiency in mice lacking the tec kinase family members tec and Btk. J Exp Med 192(11):1611-24 |
| abstractText | The cytoplasmic protein tyrosine kinase Tec has been proposed to have important functions in hematopoiesis and lymphocyte signal transduction. Here we show that Tec-deficient mice developed normally and had no major phenotypic alterations of the immune system. To reveal potential compensatory roles of other Tec kinases such as Bruton's tyrosine kinase (Btk), Tec/Btk double-deficient mice were generated. These mice exhibited a block at the B220(+)CD43(+) stage of B cell development and displayed a severe reduction of peripheral B cell numbers, particularly immunoglobulin (Ig)M(lo)IgD(hi) B cells. Although Tec/Btk(null) mice were able to form germinal centers, the response to T cell-dependent antigens was impaired. Thus, Tec and Btk together have an important role both during B cell development and in the generation and/or function of the peripheral B cell pool. The ability of Tec to compensate for Btk may also explain phenotypic differences in X-linked immunodeficiency (xid) mice compared with human X-linked agammaglobulinemia (XLA) patients. |
