Abstract In wild-type FVB mice, leukocyte recruitment to lipopolysaccharide was sexually dimorphic, with a greater number of leukocytes recruited in females. In male β 2-adrenergic receptor knock out mice (bred on a congenic FVB background) the number of leukocytes recruited was increased ∼ 4-fold, while in females there was no change, eliminating sexual dimorphism in leukocyte migration. While there were significantly fewer recruited CD62L + and CD11a + leukocytes in wild-type males, only in male β-adrenergic receptor knock out mice was there an increase in the number of recruited CD11a + leukocytes, again eliminating sexual dimorphism. Thus, leukocyte migration and CD11a + adhesion molecule expression in male, but not in female, leukocytes is β-adrenergic receptor-dependent. Our findings provide support for a role of β 2-adrenergic receptor mechanisms in the inflammatory response, and suggest that β 2-adrenergic receptor on male leukocytes contributes to sexual dimorphism in the effect of stress on inflammatory diseases.