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 Blood, 1 August 2006, Vol. 108, No. 3, pp. 904-907.
Prepublished online as a Blood First Edition Paper on March 30, 2006; DOI 10.1182/blood-2005-12-4885.

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HEMATOPOIESIS
Brief report

Identification of the nonreceptor tyrosine kinase MATK/CHK as an essential regulator of immune cells using Matk/CHK-deficient mice

Byeong-Chel Lee, Shalom Avraham, Akira Imamoto, and Hava Karsenty Avraham

From the Division of Experimental Medicine, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA; and The Ben May Institute for Cancer Research, The University of Chicago, IL.

Matk/CHK knockout mice were reported to show no apparent phenotypic abnormalities. This was thought to be due to the homologous kinase Csk that compensates for Matk/CHK. Here, we present the first evidence that the nonreceptor tyrosine kinase, Matk/CHK, is an important modulator of immune cell signaling. We found that the frequency of primitive hematopoietic cells, the side population c-kit+ Lin– Sca-1+ (SPKLS) cells, in Matk/CHK–/– mice was increased 2.2-fold compared with the control mice. Moreover, Matk/CHK deficiency led to significantly higher pre–B cell colony formation following IL-7 stimulation. Interestingly, when mice received the in vivo antigen challenge of TNP-ovalbumin followed by restimulation, the Matk/CHK–/– lymph node and spleen cells produced significantly lower IFN-{gamma} levels compared with the respective wild-type cells. Our study indicates that Matk/CHK is not functionally redundant with Csk, and that this tyrosine kinase plays an important role as a regulator of immunologic responses.


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