Moreover, the following two distinct neutrophil subsets seem to be generated in response to cryptococcal infection: (i) one with an oxidative stress signature interacting directly with the fungus and generating ROS and (ii) another with enhanced cytokine gene expression which are longer-lived and that indirectly respond to cryptococcal ligands to modulate crosstalk, via the expression of IL-1α, TNFα, and complement C3, with dendritic cells and alveolar macrophages through CCR5 and CCR1, respectively (75). Here, TNF is linked to cryptococcosis.