Here, we review the current understanding of the role of Th9/IL-9 signaling in EAE and MS. We summarize the source and regulation of Th9 cells in vivo, the influence of IL-9 signaling on peripheral and CNS-resident cells in EAE, and the association between IL-9 and MS disease activity.
Knocking down c-Rel in macrophages in vitro inhibited expression of NF-κB targets, such as pro-inflammatory cytokines interleukin 1β (IL-1β) and p40 of interleukin 12 (IL-12)/interleukin 23 (IL-23), in macrophages, leading to reduced interferon γ (IFN-γ) and interleukin 17A (IL-17A) production by co-cultured MOG-specific T cells from EAE mice.
Female C57BL/6 mice were randomly divided into three groups (n = 5 in each group): mice with myelin oligodendrocyte glycoprotein (MOG)-induced EAE (EAE group), EAE mice treated with anti-IL-9 antibody (anti-IL-9 Abs group), and EAE mice treated with IgG isotype control (IgG group).EAE clinical score was evaluated.
Furthermore, it was also demonstrated that IL-9 promotes Th17 cell-mediated tissue pathology in EAE and it compromises the barrier functions of the gut in IBD.
IL-9 targets cells of the lymphoid, myeloid and mast cell lineages, and is likely to contribute to the development of allergic and autoimmune diseases such as asthma, arthritis, multiple sclerosis and experimental autoimmune encephalomyelitis (EAE).
Therefore, we adoptively transferred myelin basic protein-specific CD4+ T cells transduced to express IL-12 p40 into mice immunized to develop experimental autoimmune encephalomyelitis and demonstrated a significant reduction in clinical disease.