Fig. 8

Proposed model for how CCR2 deficiency mediates increased neutrophil accumulation and bacterial killing. In the absence of CCR2+ monocytes, CD103+ dendritic cells respond to influenza by producing high levels of IL-6, IL-23, and IL-1β. These pro IL-17 cytokines in conjunction with decreased production of IL-27 result in robust skewing of Th17 cells as well as IL-17 secreting γδ T-cells and iNKT cells. IL-17 can activate type II alveolar epithelial cells to produce the neutrophil recruiting chemokines CXCL1/2 which promote the infiltration of bactericidal neutrophils into the lung in response to a subsequent MRSA infection