American Society of Hematology

Figure 5.

$Figure 5. S1P1–/– B cells but not S1P1–/– T cells display a defect in integrin-mediated firm arrest in PP HEVs. (A-B) The intravascular behavior of calcein-labeled B cells from S1P1+/ or S1P1–/– FL chimeras was analyzed by IVM in PP HEVs (n = 3 mice). (A) Rolling (32.1% ± 4.1% of S1P1+/ versus 24.2% ± 3.6% of S1P1–/–; **P < .01) and (B) sticking fractions (11.3% ± 1.8% of S1P1+/ versus 5.9% ± 1.3% of S1P1–/–;* P < .05). (C-D) Calcein-labeled CD4+ SP cells from S1P1+/ or S1P1–/– FL chimeras were analyzed by IVM in PP HEVs (n = 3 mice). No difference was observed in (C) rolling (37.4% ± 4.4% of S1P1+/ versus 28.4% ± 3.5% of S1P1–/–) and (D) sticking fractions (12.5% ± 2.5% of S1P1+/ versus 11.5% ± 2.8% of S1P1–/–). Error bars indicate SEM.$

S1P₁^–/– B cells but not S1P₁^–/– T cells display a defect in integrin-mediated firm arrest in PP HEVs. (A-B) The intravascular behavior of calcein-labeled B cells from S1P₁^+/ or S1P₁^–/– FL chimeras was analyzed by IVM in PP HEVs (n = 3 mice). (A) Rolling (32.1% ± 4.1% of S1P₁^+/ versus 24.2% ± 3.6% of S1P₁^–/–; **P < .01) and (B) sticking fractions (11.3% ± 1.8% of S1P₁^+/ versus 5.9% ± 1.3% of S1P₁^–/–;* P < .05). (C-D) Calcein-labeled CD4⁺ SP cells from S1P₁^+/ or S1P₁^–/– FL chimeras were analyzed by IVM in PP HEVs (n = 3 mice). No difference was observed in (C) rolling (37.4% ± 4.4% of S1P₁^+/ versus 28.4% ± 3.5% of S1P₁^–/–) and (D) sticking fractions (12.5% ± 2.5% of S1P₁^+/ versus 11.5% ± 2.8% of S1P₁^–/–). Error bars indicate SEM.

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