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However, the regulation of neutrophil adhesive function remains not fully understood. Intravital microscopy demonstrates that neutrophil DREAM promotes neutrophil recruitment to sites of inflammation induced by TNF-\u03b1 but not MIP-2 or fMLP. We observe that neutrophil DREAM represses expression of A20, a negative regulator of NF-\u03baB activity, and enhances expression of pro-inflammatory molecules and phosphorylation of I\u03baB kinase (IKK) after TNF-\u03b1 stimulation. Studies using genetic and pharmacologic approaches reveal that DREAM deficiency and IKK\u03b2 inhibition significantly diminish the ligand-binding activity of \u03b22 integrins in TNF-\u03b1\u2013stimulated neutrophils or neutrophil-like HL-60 cells. Neutrophil DREAM promotes degranulation through IKK\u03b2-mediated SNAP-23 phosphorylation. Using sickle cell disease mice lacking DREAM, we show that hematopoietic DREAM promotes vaso-occlusive events in microvessels following TNF-\u03b1 challenge. Our study provides evidence that targeting DREAM might be a novel therapeutic strategy to reduce excessive neutrophil recruitment in inflammatory diseases.<\/jats:p>","DOI":"10.1084\/jem.20211083","type":"journal-article","created":{"date-parts":[[2021,10,20]],"date-time":"2021-10-20T02:24:42Z","timestamp":1634696682000},"update-policy":"https:\/\/doi.org\/10.1084\/jem.crossmarkpolicy","source":"Crossref","is-referenced-by-count":36,"title":["Neutrophil DREAM promotes neutrophil recruitment in vascular inflammation"],"prefix":"10.1084","volume":"219","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-5626-9530","authenticated-orcid":true,"given":"Jing","family":"Li","sequence":"first","affiliation":[{"name":"Department of Pharmacology, University of Illinois at Chicago College of Medicine, Chicago, IL 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