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. Author manuscript; available in PMC: 2013 Apr 29.
Published in final edited form as: Autoimmunity. 2012 Apr 19;45(5):388–399. doi: 10.3109/08916934.2012.665523

Figure 1.

Figure 1

B6.129P2-Fcgr3tm1Sjv/J and B6;129S-Fcgr2btm1tk/J mice were obtained from Jackson Laboratories (Bar Harbor, ME) and backcrossed to B10.PL mice for three generations to generate H-2uxu mice that were then intercrossed to generate WT, heterozygous and knockout mice. EAE was induced in littermates by adoptive transfer of 1 × 106 encephalitogenic T cells generated in vitro from the spleen of B10.PL mice bearing a TCR transgene specific for MBP. Mice were scored for signs of disease daily starting on day 4 using a 5-point scale: 0- no disease; 1- tail weakness or wobbly walk; 1.5-tail weakness and wobbly walk; 2-hind limb paresis; 2.5- paralysis in one hind limb; 3- hind limb paralysis; 4-hind and forelimb paralysis and 5- death. A) Data are the mean daily scores of 24 FcγRIII+/+ and 43 FcγRIII–/ – mice from 5 separate experiments with 4-13 mice in each experiment. The FcγRIII–/ – group contains two mice that died on day 13 and 16 and were scored as 5 for the remaining timepoints. p = 0.0001. B) Data are the mean daily scores of 14 B10.PL, 9 FcγRIIb+/+, 18 FcγRIIb+/ – and 20 FcγRIIb–/ – mice from 4 separate experiments with 1-8 mice in each experiment. Mice that did not receive a score of at least 1.5 were not included in the disease curves.