Following from our previous findings that neutrophil trafficking during OPC was independent of the IL-17 pathway [6], we sought after factors responsible for controlling neutrophil recruitment in response to C. albicans. We found that mice lacking the IL-1 receptor (IL-1R) recruited significantly less neutrophils to the site of infection than their wild type (WT) counterparts (Fig 1B). This evidence concerns the gene IL1R1 and infection.