Contributions
Abstract: EP1610
Type: Poster Sessions
Abstract Category: Therapy - Immunomodulation/Immunosuppression
Dimethyl fumarate (DMF) is an oral agent for the treatment of relapsing-remitting multiple sclerosis (RRMS). The therapeutic effect of DMF has been suggested to involve neuroprotection and immunomodulation. In this study, we investigated the effect of DMF on the development of pathogenic T helper cells, type-II innate immune cells, and CNS-infiltration of pathogenic (M1) and regulatory (M2) macrophages in MOG35-55-induced experimental autoimmune encephalomyelitis (EAE) in C57BL/6 mice. DMF treatment decreased the proliferation of T cells, including MOG specific T cells, in the mesenteric lymph node (MLN) and spleen, accompanied with less differentiation of pathogenic Th17 and GM-CSF-producing Th cells. Furthermore, DMF induced a type-II innate immune response in the periphery, and significantly decreased the cell number of inflammatory macrophages (M1) and anti-inflammatory macrophages (M2) in the CNS infiltrates. The decrease in CNS-infiltrates including M1 macrophages resulted in less demyelination and axonal loss. This study suggests that DMF can promote type-II innate response and suppress the CNS-infiltration of M1 macrophages.
Disclosure: Dr. Dhib-Jalbut received Research grants from Biogen and TEVA Pharmaceuticals.
Abstract: EP1610
Type: Poster Sessions
Abstract Category: Therapy - Immunomodulation/Immunosuppression
Dimethyl fumarate (DMF) is an oral agent for the treatment of relapsing-remitting multiple sclerosis (RRMS). The therapeutic effect of DMF has been suggested to involve neuroprotection and immunomodulation. In this study, we investigated the effect of DMF on the development of pathogenic T helper cells, type-II innate immune cells, and CNS-infiltration of pathogenic (M1) and regulatory (M2) macrophages in MOG35-55-induced experimental autoimmune encephalomyelitis (EAE) in C57BL/6 mice. DMF treatment decreased the proliferation of T cells, including MOG specific T cells, in the mesenteric lymph node (MLN) and spleen, accompanied with less differentiation of pathogenic Th17 and GM-CSF-producing Th cells. Furthermore, DMF induced a type-II innate immune response in the periphery, and significantly decreased the cell number of inflammatory macrophages (M1) and anti-inflammatory macrophages (M2) in the CNS infiltrates. The decrease in CNS-infiltrates including M1 macrophages resulted in less demyelination and axonal loss. This study suggests that DMF can promote type-II innate response and suppress the CNS-infiltration of M1 macrophages.
Disclosure: Dr. Dhib-Jalbut received Research grants from Biogen and TEVA Pharmaceuticals.