Polymorphonuclear (PMN) leukocyte recruitment to sites of inflammation is initiated by selectin-mediated PMN tethering and rolling on activated endothelium under flow. Cell rolling is modulated by bulk cell deformation (meso-scale), microvillus deformability (micro-scale), and receptor-ligand binding kinetics (nano-scale). Selectin-ligand bonds exhibit a catch-slip bond behavior, and their dissociation is governed not only by the force but also the force history. Whereas previous theoretical models have studied the significance of these three "length scales" in isolation, how their interplay affects cell rolling has yet to be resolved. We therefore developed a 3D computational model that integrates the aforementioned "length scales" in order to delineate their relative contributions to PMN rolling. Our simulations predict that the catch-slip bond behavior and to a lesser extent bulk cell deformation are responsible for the shear threshold phenomenon. Cells bearing deformable rather than rigid microvilli roll slower only at high P-selectin site densities and elevated levels of shear (400 s^-1). The more compliant cells (Eh = 1.2 dyn/cm) rolled slower than cells with membrane stiffness of 3.0 dyn/cm at shear rates higher than 50^s-1. In summary, our model demonstrates that cell rolling over a ligand-coated surface is a highly coordinated process characterized by a complex interplay between forces acting on three distinct "length scales".