Autoregulatory CD8 T cells induced by Listeria-encoded neuroantigen require B cells for functional suppression of EAE 9368

Description Myelin-reactive CD8 T cells (CD8s) have unexpected regulatory potential in MS and its mouse model experimental autoimmune encephalomyelitis (EAE). Previous work studied endogenous generation of these autoregulatory CD8s in mice, where infection with an intracellular bacterium Listeria monocytogenes engineered to express a myelin proteolipid protein sequence (LM-PLP) robustly protected from EAE. This protection was dependent on CD8s. Interestingly, reports suggest B cells aid in CD8 memory formation against LM. We hypothesized that B cells may influence induction of autoregulatory CD8s by LM-PLP. Here, we show that infection with LM-PLP fails to protect against EAE in mice lacking B cells and demonstrate that adoptive transfer of CD8s sourced from LM-PLP infected donors robustly protect recipients from EAE but fails to do so if donor mice lacked B cells. These preliminary results highlight a critical role for B cell:CD8 T cell interactions in this model. Ongoing experiments are characterizing these interactions (whether direct or indirect), phenotyping CD8s, and identifying potential B cell mechanisms influencing LM-PLP induced, EAE-suppressive, autoregulatory CD8 T cells.