This record contains raw data related to article "Neutrophils mediate protection in colitis and carcinogenesis by controlling bacterial invasion and IL-22 production by gd T cells" Abstract Neutrophils are the most abundant leukocytes in human blood and play a primary role in resistance against invading microorganisms and in the acute inflammatory response. However, their role in colitis and colitis-associated colorectal cancer is still under debate. Therefore, this study aims to dissect the role of neutrophils in these pathological contexts by using a rigorous genetic approach. Neutrophil-deficient mice (Csf3r-/- mice) were challenged with classic models of colitis and colitis-associated colorectal cancer and the role of neutrophils was assessed by histological, cellular and molecular analyses coupled with adoptive cell transfer and correlative analyses using human datasets. Csf3r-/- mice showed increased susceptibility to colitis and colitis-associated colorectal cancer compared to control Csf3r+/+ mice and adoptive transfer of neutrophils in Csf3r-/- mice reverted the phenotype. In colitis, Csf3r-/- mice showed increased bacterial invasion and reduced number of healing ulcers in the colon, indicating compromised regenerative capacity of epithelial cells. Neutrophils were essential for  T cell polarization and IL-22 production. In patients with ulcerative colitis, the expression of CSF3R was positively correlated with IL-22 and IL-23 expression. Moreover, gene signatures associated with epithelial cell development, proliferation and antimicrobial response were enriched in CSF3Rhigh patients. Our data support a model where neutrophils mediate protection against intestinal inflammation and colitis-associated colorectal cancer by controlling the intestinal microbiota and driving the activation of an IL-22-dependent tissue repair pathway.