TLR9 and experimental autoimmune encephalomyelitis: B10 cells have been demonstrated to be potent regulators of allergic and autoimmune disease, transplant rejection, infection and cancer.28 It has been reported that the adoptive transfer of B10 cells induced by LPS (lipopolysaccharide, TLR4 agonist) or CpG ODN1826 (oligodeoxynucleotide, TLR9 agonist) reduced the severity of EAE (experimental autoimmune encephalomyelitis) via suppressing IFN‐γ and IL‐17 production by CD4+ T cells.29, 30 In the current study, ManLAM‐induced B10 cells suppressed the IFN‐ γ production by CD4+ T cells, but did not change the IL‐17 production (Figures 4 and 5).