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. 2015 May 15;180(3):419–431. doi: 10.1111/cei.12594

Fig 1.

Fig 1

rTl-gal treatment increased the clinical symptoms of experimental autoimmune encephalomyelitis (EAE). (a) Clinical scores of myelin oligodendrocyte glycoprotein (MOG)-induced EAE in recombinant Toxascaris leonine galectin (rTl-gal)- and vehicle-treated mice. rTl-gal showed higher mean clinical scores than vehicle-treated control mice. A representative of six independent experiments is shown, in which each data point represents the mean ± standard error of the mean (s.e.m.) of 27 vehicle and 20 rTl-gal-treated mice. Arrows indicate days of rTl-gal injection. (b) rTl-gal treatment stimulated the proliferation of splenic mononuclear cells to MOG35–55 restimulation at chronic stage. Proliferative response to the antigens [MOG35–55, proteolipid protein (PLP)138–151 or concanavalin A (ConA)] was assessed in triplicate wells for each experiment. Background proliferation was 729 ± 245 counts per minute (cpm) and concanavalin A (ConA)-induced proliferation was 42 986 ± 5737 cpm. Data are the mean ± s.e.m. of cpm and are representative of three independent experiments. Statistical evaluation was performed to compare the experimental groups and corresponding control groups, respectively. *P < 0·05.