Skip to main content
. Author manuscript; available in PMC: 2011 Jun 1.
Published in final edited form as: J Autoimmun. 2009 Dec 24;34(4):453–459. doi: 10.1016/j.jaut.2009.11.017

Figure 4. γC399tr protects mice from actively induced EAE.

Figure 4

Sixteen C57BL/6 mice were immunized subcutaneously with MOG p:35-55 in an encephalitogenic fashion. On day 4, mice were randomly divided into two groups of eight mice each. One group received daily injections of 100 μg of γC399tr while the other group received an equal volume of refolding buffer alone. The degree of paralysis was then scored daily as described in the materials and methods. On day 16, treatments were crossed; animals initially receiving refolding buffer started to receive γC399tr and vice versa. Treatment injections were given in the morning and animals scored blindly in the evening. Averages for each group are graphed as days post injection versus EAE disease score. 4A) Upper left- seven of eight mice receiving control treatments with buffer alone developed EAE. 4B) Upper right- mice receiving γC399tr treatment were protected from EAE induction (0/8) (P<0.00001, student T test). 4C) Lower left- once animals developed EAE i.p. treatments with γC399tr could reverse their active disease. 4D) Lower right- four of the eight mice that were initially protected by γC399tr treatments developed EAE once this therapy was switched to refolding buffer.