Removing either MyD88 or the signaling pathways regulated by it (TLRs and IL-1ß) from bone marrow-derived cells significantly inhibited diabetes-induced defects in the retina, including leukostasis, ICAM-1 expression on the luminal surface of the vascular endothelium, retinal superoxide generation, and leukocyte-mediated killing of endothelial cells. This evidence concerns the gene IL1B and diabetes mellitus.