Figure 6.
S1PR5-deficiency results in altered NK and ILC1 tissue distribution. (A) Heatmap represents of gene expression (z-score normalized by row) of mouse NK and ILC1 cells isolated from spleen, liver, and SI-IEL. Gene expression was extracted from the ImmGen Consortium (GEO under accession no. GSE37448). (B and C) WT (CD45.1+CD45.2+) and S1pr5−/− (CD45.2+) BM cells were cotransferred at a 1:1 ratio into lethally irradiated CD45.1 recipient mice. Donor-derived (CD45.2+) NK and ILC1 cells were analyzed from indicated organs >8 wk after transfer. Shown are relative frequencies of WT and S1pr5−/− of NK and ILC1 cells (B) and corresponding gating strategies (C). Data are representative of three independent experiments, with n = 9–10 per experiment. ****, P < 0.0001 by two-way ANOVA. n.s., not significant; SG, salivary gland; Spl., spleen.

S1PR5-deficiency results in altered NK and ILC1 tissue distribution. (A) Heatmap represents of gene expression (z-score normalized by row) of mouse NK and ILC1 cells isolated from spleen, liver, and SI-IEL. Gene expression was extracted from the ImmGen Consortium (GEO under accession no. GSE37448). (B and C) WT (CD45.1+CD45.2+) and S1pr5−/− (CD45.2+) BM cells were cotransferred at a 1:1 ratio into lethally irradiated CD45.1 recipient mice. Donor-derived (CD45.2+) NK and ILC1 cells were analyzed from indicated organs >8 wk after transfer. Shown are relative frequencies of WT and S1pr5−/− of NK and ILC1 cells (B) and corresponding gating strategies (C). Data are representative of three independent experiments, with n = 9–10 per experiment. ****, P < 0.0001 by two-way ANOVA. n.s., not significant; SG, salivary gland; Spl., spleen.

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