Immune modulation by Lacto-N-fucopentaose III in experimental autoimmune encephalomyelitis

Parasitic infections frequently lead to immune deviation or suppression. However, the application of specific parasitic molecules in regulating autoimmune responses remains to be explored. Here we report on the immune modulatory function of Lacto-N-fucopentaose III (LNFPIII), a schistosome glycan, in an animal model for multiple sclerosis. We found that LNFPIII treatment significantly reduced the severity of experimental autoimmune encephalomyelitis (EAE) and CNS inflammation, and skewed peripheral immune response to a Th2 dominant profile. Inflammatory monocytes (IMCs) purified from LNFPIII-treated mice had increased expression of nitric oxide synthase 2, and mediated T cell suppression. LNFPIII treatment also significantly increased mRNA expression of arginase-1, aldehyde dehydrogenase 1 subfamily A2, indoleamine 2,3-dioxygenase and heme oxygenase 1 in splenic IMCs. Furthermore, LNFPIII treatment significantly reduced trafficking of dendritic cells across brain endothelium in vitro. In summary, our study demonstrates that LNFPIII glycan treatment suppresses EAE by modulating both innate and T cell immune response.

► Lacto-N-fucopentaose III (LNFPIII) is a schistosome glycan.
► LNFPIII treatment reduced severity of experimental autoimmune encephalomyelitis.
► LNFPIII treatment skewed peripheral immune response to a Th2 dominant profile.
► LNFPIII treatment induced immune regulatory enzymes in inflammatory monocytes.
► LNFPIII treatment reduced trafficking of dendritic cells across brain endothelium.