Figure 5
Figure 5. VEGF-A expression and inhibition during LCMV-induced PLN remodeling. (A) qPCR analysis of VEGF-A and VEGFR2 expression in LCMV-infected PLNs. Two PLNs from 2 mice per time point were analyzed in duplicates. (B) Experimental layout for VEGF signaling blocking and LCMV infection in WT mice. Mice received 2 injections on day 0 and 3 after infection of Abs as described in “In vivo antibody and inhibitor treatment” or daily gavage of the VEGFR/PDGFR-inhibitor sunitinib. (C) Inguinal LN volume on day 0 (D0) or day 8 (D8) after infection after treatment of mice with control Ig or anti-VEGFR2, anti–VEGF-A Abs, or sunitinib. Examples were pooled from 1 to 2 independent experiments with 3 to 5 mice per treatment. (D) Total HEV length on day 0 (D0) or day 8 (D8) after infection as in panel C. No significant difference was found in panels C and D between day 8 control Ig and Ab- or inhibitor-treated values (1-way ANOVA).

VEGF-A expression and inhibition during LCMV-induced PLN remodeling. (A) qPCR analysis of VEGF-A and VEGFR2 expression in LCMV-infected PLNs. Two PLNs from 2 mice per time point were analyzed in duplicates. (B) Experimental layout for VEGF signaling blocking and LCMV infection in WT mice. Mice received 2 injections on day 0 and 3 after infection of Abs as described in “In vivo antibody and inhibitor treatment” or daily gavage of the VEGFR/PDGFR-inhibitor sunitinib. (C) Inguinal LN volume on day 0 (D0) or day 8 (D8) after infection after treatment of mice with control Ig or anti-VEGFR2, anti–VEGF-A Abs, or sunitinib. Examples were pooled from 1 to 2 independent experiments with 3 to 5 mice per treatment. (D) Total HEV length on day 0 (D0) or day 8 (D8) after infection as in panel C. No significant difference was found in panels C and D between day 8 control Ig and Ab- or inhibitor-treated values (1-way ANOVA).

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