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The Journal of Experimental Medicine
Year: 2009  |  Volume: 206  |  Issue: 11  |  Page No.: 2469 - 2481

T-bet-dependent S1P5 expression in NK cells promotes egress from lymph nodes and bone marrow

C. N Jenne, A Enders, R Rivera, S. R Watson, A. J Bankovich, J. P Pereira, Y Xu, C. M Roots, J. N Beilke, A Banerjee, S. L Reiner, S. A Miller, A. S Weinmann, C. C Goodnow, L. L Lanier, J. G Cyster and J. Chun    

Abstract:

During a screen for ethylnitrosourea-induced mutations in mice affecting blood natural killer (NK) cells, we identified a strain, designated Duane, in which NK cells were reduced in blood and spleen but increased in lymph nodes (LNs) and bone marrow (BM). The accumulation of NK cells in LNs reflected a decreased ability to exit into lymph. This strain carries a point mutation within Tbx21 (T-bet), which generates a defective protein. Duane NK cells have a 30-fold deficiency in sphingosine-1-phosphate receptor 5 (S1P5) transcript levels, and S1P5-deficient mice exhibit an egress defect similar to Duane. Chromatin immunoprecipitation confirms binding of T-bet to the S1pr5 locus. S1P-deficient mice exhibit a more severe NK cell egress block, and the FTY720-sensitive S1P1 also plays a role in NK cell egress from LNs. S1P5 is not inhibited by CD69, a property that may facilitate trafficking of activated NK cells to effector sites. Finally, the accumulation of NK cells within BM of S1P-deficient mice was associated with reduced numbers in BM sinusoids, suggesting a role for S1P in BM egress. In summary, these findings identify S1P5 as a T-bet–induced gene that is required for NK cell egress from LNs and BM.

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