This protection is dually dependent on IgG-FcγR signalling and CD4+ T cells, but independent of secretory IgA.10,61,62 It is noteworthy that Nod2-deficient mice, which are susceptible to C. rodentium challenge, exhibit an impaired local anti-microbial IgG response, suggesting local IgG dysfunction may compound invasive bacterial dissemination that precipitates colitis.63 In addition, although anti-microbial IgG is elevated in CD patients, the quality and nature of this response is likely to vary according to individual genetic and environmental factors. Here, FCGR2A is linked to colitis.