Given these findings, an absence of IL-1β in neutrophil-depleted mice following influenza infection would suggest that either neutrophils are the sole source of this cytokine or that they indirectly mediate IL-1β expression and/or release in other hematopoietic populations (most likely alveolar macrophages, given previous literature).15 20 23–25 We subsequently assessed the relative capacity of these candidate cell types to produce IL-1β. The gene discussed is IL1B; the disease is influenza.