It has been discovered that NO actively engages in the IgA production pathways that are T cell-independent (TI) and T cell-dependent (TD). More specifically, NO aids in the TD route by causing the type II TGF-β receptor to surface on B cells, which in turn promotes the synthesis of IgA. Within the TI route, NO triggers the production of two unique proteins, APRIL and BAFF, which are essential for the maturation of IgA+ B cells. When NO is present, certain cells (CX3CR1+) produce these proteins. They further aid in the conversion of IgM+ B cells into IgA+ B cells, which subsequently progress into plasma cells that produce IgA. Furthermore, through inducing CCR7, NO influences the migration of DC cells towards the mesenteric lymph nodes.