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.
Bibliographical noteFunding Information:
This work was supported by the National Institutes of Health grants ( RO1AI058680 , RO1AI067472 to S. J. Khoury and 1R21AI076794 to I. Guleria), Juvenile Diabetes Research Foundation grant ( 1-2007-756 to I. Guleria) and the National Multiple Sclerosis Society grants ( RG-3945 to S. J. Khoury, RG-4278 to B. Zhu).
Copyright 2012 Elsevier B.V., All rights reserved.
- Experimental autoimmune encephalomyelitis
- Immune modulation