Figure 2 Glatiramer acetate treatment induced M2 differentiation through a MyD88-independent pathway (A) As described previously,3 M2 monocytes were treated.

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Figure 2 Glatiramer acetate treatment induced M2 differentiation through a MyD88-independent pathway (A) As described previously,3 M2 monocytes were treated in the presence or absence of glatiramer acetate (GA) for 6 days. Glatiramer acetate treatment induced M2 differentiation through a MyD88-independent pathway (A) As described previously,3 M2 monocytes were treated in the presence or absence of glatiramer acetate (GA) for 6 days. They were then stimulated with lipopolysaccharide (LPS), Poly(I:C), or Pam3CSK4 for 24 hours. (B) Wild-type (WT) monocytes cultured in the presence or absence of GA were stimulated with LPS (100 ng/mL) for the indicated duration. Cell lysate proteins were separated by sodium dodecyl sulfate polyacrylamide gel electrophoresis and membranes were probed for phosphorylated IκBα (Ser32/36). Data are representative of 2 separate experiments. (C) Human peripheral blood monocytes were preincubated for 1 hour with or without 50 μg/mL GA and then cultured for 24 hours in the presence or absence of Poly(I:C) (10 μg/mL) or Pam3CSK4 (100 ng/mL). Tumor necrosis factor (TNF) (left panels) and interleukin (IL)–6 (right panels) secretion was quantitated in cell supernatants by ELISA. Results are presented as mean ± SD (n = 3); **p < 0.01, ***p < 0.001 by Student t test. Data presented are representative of 3 independent experiments. MyD88 = myeloid differentiation primary response gene 88; TRIF = Toll-IL-1 receptor domain–containing adaptor inducing interferon-β. Nicolas Molnarfi et al. Neurol Neuroimmunol Neuroinflamm 2015;2:e179 © 2015 American Academy of Neurology