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Published online 4 December 2000.
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© The Rockefeller University Press, 0022-1007/2000/12/1611/ $5.00
The Journal of Experimental Medicine, Volume 192, Number 11, December 4, 2000 1611-1624

Original Article

Severe B Cell Deficiency in Mice Lacking the Tec Kinase Family Members Tec and Btk

Wilfried Ellmeiera,b, Steffen Junga, Mary Jean Sunshinea,b, Farah Hatama,b, Yang Xuc, David Baltimored, Hiroyuki Manoe, and Dan R. Littmana,b
a Molecular Pathogenesis Program, Skirball Institute of Biomolecular Medicine,
b Howard Hughes Medical Institute, New York University School of Medicine, New York, New York 10016
c Department of Biology, University of California at San Diego, San Diego, California 92093
d Office of the President, California Institute of Technology, Pasadena, California 91125
e Division of Functional Genomics, Jichi Medical School, Tochigi 329-0498, Japan

Correspondence to: Wilfried Ellmeier, Institute of Immunology, University of Vienna, Brunner Strasse 59, 1235 Vienna, Austria. Tel:43-1-4277-64986 Fax:43-1-4277-64991 E-mail:wilfried.ellmeier{at}univie.ac.at.

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)MloIgDhi B cells. Although Tec/Btknull 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.

Key Words: gene targeting, B cell development, lymphocytes, signaling, X-linked immunodeficiency


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