Together, these findings support a model in which iron mishandling at level of the mucosal lining in colonocytes is a likely catalyst of peripheral (blood and gut) immune dysfunction evident in both IBD and PD, as measured by downregulation of key regulatory immune response genes in a colonocyte subpopulation that is actively transcribing ferritin genes to deal with iron overload, dynamically increasing interactions with IgA-producing plasma cells, and upregulating antigen-presenting complexes that induce cytotoxic T cell differentiation. This evidence concerns the gene CD79A and Parkinson disease.