Pulmonary immunity to fungal pathogens requires both innate and adaptive immune responses. Alveolar macrophages, dendritic cells, and neutrophils are the phagocytic cells of the lung innate system. These cells produce early inflammatory mediators (i.e., reactive oxygen species, cytokines, and chemokines) in response to fungal infection. The production of early cytokines by innate cells, namely tumor necrosis factor alpha (TNF-alpha) and interleukin (IL)-12, plays a central role in the development of protective cell-mediated immunity against fungi. T helper 1 (Th1) cell-mediated immunity is essential for limiting a pulmonary fungal infection. Virulence factors produced by the fungi can also modulate the host immune response. Fungal virulence factors include the production of prostaglandins and a polysaccharide capsule. The type of adaptive immune response (T1 vs T2) generated determines whether the fungi are cleared from the lungs or a chronic fungal infection prevails.