Therefore, we propose that in CGD the crucial positive-feedback loop consisting of the secretion of anti-inflammatory IL-4 by macrophages does not take place, and pro-inflammatory M1 macrophages cannot develop into anti-inflammatory M2a macrophages, as this step requires exposure to anti-inflammatory cytokines such as IL-4 and IL-13 (45, 46). Here, IL13 is linked to chronic granulomatous disease.