In chronic infections like HIV (13) and malaria (14), and also in autoimmune diseases like rheumatoid arthritis (15) and systemic lupus erythematosus (16), there is upregulation of inhibitory and proapoptotic receptors on B cells coupled with increased frequency of a phenotypically distinct MBC subset lacking the classic memory marker CD27 (2, 3, 17, 18) and usually accompanied by an increase of IgD−CD27+ classical MBC (19–21). Here, CD27 is linked to malaria.