Physiological studies with human leukocyte inhibitory factor

LIF has been shown to be a potentially important activator of neutrophil function. By means of its dose-dependent dichotomous effects on chemotaxis, LIF can be predicted to both enhance the potency of chemotactic stimuli and promote the passive accumulation of PMN at inflammatory loci. Furthermore, LIF's stimulatory effects on both PMN- and endothelial cell-mediated adherence will promote the migration of neutrophils from the circulation to the inflammatory site. We have demonstrated LIF stimulation of fMLP, CR1, and CR3 expression and function, as well a stimulated Fc gamma RIII function. Through both receptor-dependent and -independent effects. LIF produces increased target cell attachment, phagocytosis, respiratory burst activity, and degranulation. Together, these effects result in a significant increase in killing of both phagocytosed targets and extracellular targets.