To analyze the effect of IL-1R signaling on T cell differentiation during infection, we harvested lungs at serial time points, restimulated the cells with PMA/ionomycin, and stained for intracellular IFNγ, IL-13, and IL-17A as representative cytokines for Th1, Th2, and Th17 polarization states, respectively (Figure 9). The gene discussed is IL1R1; the disease is infection.