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 Blood, 1 July 2008, Vol. 112, No. 1, pp. 131-140.
Prepublished online as a Blood First Edition Paper on March 12, 2008; DOI 10.1182/blood-2007-08-107847.

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IMMUNOBIOLOGY

Enhanced NK-cell development and function in BCAP-deficient mice

Alexander W. MacFarlane, IV1, Tetsuo Yamazaki2, Min Fang1, Luis J. Sigal1, Tomohiro Kurosaki3, and Kerry S. Campbell1

1 Fox Chase Cancer Center, Division of Basic Science, Institute for Cancer Research, Philadelphia, PA; 2 Kyoto University Graduate School of Pharmaceutical Sciences, Kyoto, Japan; and 3 Laboratory for Lymphocyte Differentiation, RIKEN Research Center for Allergy and Immunology, Yokohama, Japan

In B lymphocytes, the B-cell adaptor for phosphatidylinositol 3-kinase (BCAP) facilitates signaling from the antigen receptor. Mice lacking BCAP have a predominantly immature pool of B cells with impaired immune function and increased susceptibility to apoptosis. Unexpectedly, we have found that natural killer (NK) cells from BCAP-deficient mice are more mature, more long-lived, more resistant to apoptosis, and exhibit enhanced functional activity compared with NK cells from wild-type mice. Surprisingly, these effects are evident despite a severe impairment of the immunoreceptor tyrosine-based activation motif-mediated Akt signaling pathway. The seemingly paradoxical phenotype reveals inherent differences in the signals controlling the final maturation of B cells and NK cells, which depend on positive and negative signals, respectively. Both enhanced interferon-{gamma} responses and augmented maturation of NK cells in BCAP-deficient mice are independent of available MHC class I ligands. Our data support a model in which blunting of BCAP-mediated activation signaling in developing NK cells promotes functionality, terminal maturation, and long-term survival.


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Related Article in Blood Online:

Inhibitions in NK-cell maturation
Werner Held
Blood 2008 112: 8-9. [Full Text] [PDF]





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