ITGAM and coronary artery disorder: This reduced response to C3bi-opsonised yeast might also reflect the adhesive property of the β2-integrin [26], but regardless of whether the observed down-regulated signalling capacity was due to a dysfunctional signalling capacity per se or resulted from decreased adhesion, the results indicate that inside-out signalling regulating CD11b/CD18-integrin avidity was down-regulated in patients with stable CAD.