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. 2013 Nov 17;2013:268486. doi: 10.1155/2013/268486

Figure 2.

Figure 2

((a)–(g)) C16 treatment attenuated the CD4+ lymphocytes extravasation in CNS both at weeks 2 and 8 after immunization. CD4 immunostaining, counterstained with hematoxylin; bar = 100 μm. At week 2 after immunization, normal group (a), vehicle control rats (b) (with severe cellular infiltration within parenchyma and surrounding blood vessel), 1 mg /day C16 treated EAE rats (c), C16 late treated EAE rats (d) (the arrow denotes “perivascular cuffing” of CD4+ lymphocyte). At week 8 after immunization, vehicle control rats (e), and 1 mg/per day C16 treated EAE rats (f), and C16 late treated EAE rats (g). ((h)–(j)) The C16 treatment attenuated the leukocytes infiltration in CNS both at weeks 2 and 8 after immunization. TRITC conjugated CD45 immunofluorescent staining. At week 2 after immunization, vehicle control rats (h), 2 mg/per day C16 treated EAE rats (i), and C16 late treated EAE rats (j). ((k)–(p)) The C16 treatment attenuated macrophages extravasation in CNS both at weeks 2 and 8 after immunization. TRITC conjugated CD68 immunofluorescent staining. At week 2 after immunization, vehicle control rats (k), 2 mg/per day C16 treated EAE rats (l), and C16 late treated EAE rats (m). At week 8 after immunization, vehicle control rats (n), 2 mg/day C16 treated EAE rats (o), and C16 late treated EAE rats (p).