This article dedicated to Ines Mandl at her 80th birthday is a short review of the recent work of our team on the elastin receptor. Our studies started in the early nineteen eighties aimed at the understanding of cell-elastin interactions. The first experiments reviewed demonstrated the inducible interaction of cells - smooth muscle cells, fibroblasts - with elastic fibers. Their strong adhesion was accelerated and amplified by elastin peptides and cell adhesion to elastin needed protein neosynthesis. The demonstration of the presence of the elastin receptor on leukocytes facilitated the detailed description of the transmission pathway from receptor to the intracellular sites activated by the receptor: modifications of ion fluxes, increase of elastase production and excretion of reactive oxygen species, superoxide and NO°. The calcium transients triggered by elastin peptides acting on the receptor decrease with age, the receptor appears to be uncoupled from the G-proteins, but superoxide release is increased. As circulating blood was shown to contain elastin peptides at concentrations saturating for the receptor (μg/ml conc-s for a Kd in the nanomolar range), the receptor on cells in contact with excess agonists is constantly overstimulated. The continuous release of lytic enzymes and free radicals might well be involved in cell damage. This was demonstrated with human lymphocytes undergoing cell death by necrosis and apoptosis in presence of higher concentrations of elastin peptides.