Fig. 6.
Schematic illustration summarizes the cytokine loop that causes neutrophilia in IkkβΔ mice. In response to normal levels of circulating TNF-α, Ikkβ-deficient myeloid progenitors (CMP and GMP) undergo rapid apoptosis and thereby release IL-1β, which leads to elevated plasma IL-6. Increased IL-1β and IL-6, together with physiological levels of TGF-β and IL-23, induce a Th17 polarization of CD4+ cells that is responsible for further amplification of IL-6 as well as the induction of G-CSF, which subsequently causes a compensatory expansion of GMP that ultimately culminates in granulocytosis.