Key findings include that (1) stroke induces marked loss of splenic MZ B cells along with gross disruption to splenic microarchitecture, (2) MZ B-cell capture of antigen is deficient after stroke, (3) circulating IgM levels are suppressed after stroke in mice and humans and lower IgM levels are evident in stroke patients with infection and (4) β2-AR-mediated signalling drives stroke-induced MZ B-cell loss and susceptibility to infection. Here, CD40LG is linked to infection.