Alternatively, IgA-producing plasma cells have been shown to migrate out of their niche and into the CNS in an attempt to regulate neuroinflammation in a mouse model of experimental autoimmune encephalomyelitis.62 Furthermore, gut re-colonization of germ-free mice leads to an increase in meningeal plasma cells, whose B-cell receptor sequencing has confirmed their intestinal origin.63 However, mature antibody-secreting plasma cells normally downregulate CD2064 and TG2-specific plasma cells in the gut of CD patients have been shown to be CD20−65. Here, CD79A is linked to experimental autoimmune encephalomyelitis.