Figure 2.

We propose (i) that SR-Ab_B-2 alongside non-Self Abs_B-2 were originally produced from NAAb_B-1a-like receptors and (ii) that the present-day production of B2-cell-derived Abs is enhanced in environments where NAAb_B-1a’ production—chiefly taking place during fetal/neonatal period—and/or activity are reduced. Acting as first line of defense, the production of NAAb_B-1a is enhanced in environments with a high incidence of infection. This excess of NAAb_B-1a protects from ADs whereas the limited production of SR-Ab_B-2 reduces the risk for ADs. In environments with a low incidence of infection the relative excess of SR-Ab_B-2 alongside the reduction of NAAb_B-1a enhance the risk of developing ADs