MICROVASCULAR proliferation is essential to many biological processes, such as wound healing, but the mechanisms underlying this vascular response are poorly understood¹. Neovascularisation can be induced by extracts from various cell types, including malignant solid tumour cells², normal and viral-transformed (SV40) BALB/c 3T3 cells, and diploid human embryonic lung fibroblasts³, and neutrophils⁴. Extracts of mouse salivary gland⁵ and skin⁶ have been reported to induce vascular growth, but the relevance of these observations to the vascular proliferation that occurs in wound healing and chronic inflammation is unclear. Neovascularisation is also an important component of immunological reactions. Sidky and Auerbach reported increased vessel density in the skin during graft-versus-host reactions and attributed it to the lymphocyte⁷. Herman and associates⁸ and Anderson et al.⁹ found an increase in capillary density, and extensive proliferation of postcapillary venular endothelium, respectively, in lymph nodes undergoing strong immunological reactions. We have shown significant endothelial proliferation in delayed hypersensitivity reactions in the skin of guinea pigs at the time of maximal mononuclear cell infiltration¹⁰ and so we have investigated whether macrophages, an important component of immunological and non-immunological inflammatory reactions, might be involved in this vascular response. We report here that macrophages activated in vivo and in vitro, and media conditioned by these cells, induce vascular proliferation in the guinea pig cornea.