A study on CCL28-deficient mice showed an abnormal distribution and reduction in IgA-ASCs in the lamina propria of the colon and decreased IgA production capacity, resulting in aggravated dextran sulfate sodium (DSS)-induced colitis and an increased frequency of bacterial infiltration into the lamina propria of the colon compared to wild-type mice [82]. This evidence concerns the gene CD79A and colitis.