Blockade of VEGF-A, but not of VEGF-C, inhibits inflammation-induced LN lymphangiogenesis. A DTH response to oxazolone was induced in the ears of WT mice and maintained by repeatedly applying oxazolone for 9 days. Mice with inflamed ears were exposed to anti–VEGF-A Ab (A-F), VEGFR3-Fc (G-L), or control IgG (A-L), and the effects were compared with those observed in mice in which inflammation had not been induced (ctr). (A-F) Effect of anti–VEGF-A: Weight (A) and cellularity (B) of the auricular LN was significantly increased in mice with inflamed ears, exposed to anti–VEGF-A or IgG. This effect was less pronounced in inflamed LNs of mice that had been administered anti–VEGF-A compared with IgG. (C) Exposure to anti–VEGF-A potently blocked the increase in LEC numbers in LNs draining inflamed ears, whereas exposure to IgG had no effect. (D) Inflammation led to a significant increase in leukocyte numbers in the ears of both anti–VEGF-A or IgG treated mice, compared with uninflamed the ears of control animals. (E, F) Administration of anti–VEGF-A potently blocked the increase in LEC (E) and BEC (F) numbers in inflamed ears of mice. (G-L) Effect of VEGFR3-Fc: Weight (G) and cellularity (H) of the auricular LN was similarly increased in mice with inflamed ears exposed to VEGFR3-Fc or IgG. (I) Administration of VEGFR3-Fc did not block the increase in LEC numbers in LNs draining inflamed ears. (J) Leukocyte numbers were strongly increased in inflamed ears of mice exposed to IgG. Administration of VEGFR3-Fc led to a significant reduction in the numbers of leukocytes in inflamed ears. Administration of VEGFR3-Fc had no effect on the numbers of LECs (K) or BECs (L) in inflamed ears of mice. *P < .05, **P < .01, ***P < .001 (compared with control [ctr]); #P < .05, ##P < .01, ###P < .001 (anti–VEGF-A or VEGFR3-Fc, compared with IgG). Error bars are SE.