CD163 and Stroke: Collectively, our findings infer a mechanism in which peripherally circulating factors induced by stroke trigger ADAM17-dependant CD163 shedding by monocytes, driving an increase in sCD163 levels which act to suppress peripheral lymphocyte activity; this mechanism likely serves as a means of maintaining self-tolerance as the blood brain barrier becomes disrupted and peripheral lymphoid populations become exposed to activated innate antigen presenting cells loaded with unfamiliar neural antigens (Fig. 6).