A novel B cell-driven EAE mouse model reveals the impact of B cell-derived cytokines on CNS autoimmunity

We developed an adjuvant-free co-transfer EAE mouse model, in which highly activated, MOG-specific induced germinal center B (iGB) cells provide the critical stimulus for disease development. As our model allows for B cell manipulation prior to transfer, we found that overexpression of IL-6 leads to an accelerated EAE onset accompanied by activation/expansion of the myeloid compartment even in mice that received non-specific polyclonal iGB cells. To analyze the effects of IL-6 overexpression on the myeloid compartment, we compared CD11b+ cells from mice that received polyclonal WT iGB cells overexpressing IL-6 (WT iGB6) and mice that received MOG-specific B cells transduced with an empty vector (IgHMOG iGBGFP) by RNAseq. Overall design: RNAseq from CD11b+ cells isolated from WT iGB6 recipients vs. CD11b+ cells from IgHMOG iGBGFP recipients (n=3 mice/group).