The suppressor of cytokine signalling 3 (SOCS3) protein is part of a negative feedback loop that controls signalling by several key cytokines such as IL-6, G-CSF and IL-1β. Through this mechanism, SOCS3 regulates important cellular processes such as haematopoiesis and inflammation, ensuring that they are maintained at homeostatic levels. To complement studies carried out in mammalian models, the function of the zebrafish socs3b orthologue was investigated. A global gene knockout was generated using CRISPR/Cas9, which unlike the mouse Socs3 knockout was viable, providing a opportunity to study the impacts of global SOCS3 ablation throughout the life course. Zebrafish socs3bknockout embryos displayed elevated levels of myeloid progenitors during primitive hematopoiesis and an increase in neutrophils during definitive hematopoiesis. During adulthood, socs3b knockout zebrafish developed an inflammatory phenotype characterized by uveitis, with extensive infiltration of neutrophils and macrophages into the eye. Infiltration of neutrophils was also observed in several other tissues such as kidney and spleen. Wounding assays conducted on embryos further revealed that macrophages were more active in the mutants, with an elevation in chemokine markers. These findings identify a conserved role for socs3b in the regulation of neutrophil production and inflammation, including an additional role in the activation of embryonic macrophages.