Despite the fact that SIgA2 showed a slightly higher ability to accelerate bacterial shedding at early stage of infection in comparison to the SIgA1 counterpart (Figure 4A), differences in length and glycosylation of the hinge region between the two human IgA isotypes do not appear to significantly undermine the ability of the polymeric immunoglobulins to prevent inflammation (Figures 4B–D). The gene discussed is CD79A; the disease is infection.