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 Blood, 5 November 2009, Vol. 114, No. 19, pp. 4081-4088.
Prepublished online as a Blood First Edition Paper on September 8, 2009; DOI 10.1182/blood-2009-05-219881.

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IMMUNOBIOLOGY

Fibronectin maintains survival of mouse natural killer (NK) cells via CD11b/Src/β-catenin pathway

Ting Zhang1,2,*, Shuxun Liu2,*, Pengyuan Yang2, Chaofeng Han2, Jianli Wang1, Juan Liu2, Yanmei Han2, Yizhi Yu2, and Xuetao Cao1,2

1 Institute of Immunology, Zhejiang University School of Medicine, Hangzhou; and 2 National Key Laboratory of Medical Immunology & Institute of Immunology, Second Military Medical University, Shanghai, People's Republic of China

Tissue microenvironment and stroma-derived extracellular matrix (ECM) molecules play important roles in the survival and differentiation of cells. Mouse natural killer (NK) cells usually die within 24 hours once isolated ex vivo. Exogenous cytokines such as interleukin-12 (IL-12) and IL-15 are required to maintain the survival and activity of mouse NK cells cultured in vitro. Whether and how ECM molecules such as fibronectin can support the survival of NK cells remain unknown. We demonstrate that fibronectin, just like IL-15, can maintain survival of mouse NK cells in vitro. Furthermore, we show that fibronectin binds to the CD11b on NK cells, and then CD11b recruits and activates Src. Src can directly interact with β-catenin and trigger nuclear translocation of β-catenin. The activation of β-catenin promotes extracellular signal-related kinase (ERK) phosphorylation, resulting in the increased expression of antiapoptotic protein B-cell leukemia 2 (Bcl-2), which may contribute to the maintenance of NK-cell survival. Consistently, fibronectin cannot maintain the survival of CD11b– NK cells and β-catenin–deficient NK cells in vitro, and the number of NK cells is dramatically decreased in the β-catenin–deficient mice. Therefore, fibronectin can maintain survival of mouse NK cells by activating ERK and up-regulating Bcl-2 expression via CD11b/Src/β-catenin pathway.


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