Neovascularisation is the principal vascular response in chronic inflammation. The role of angiogenesis in pathogenesis of interstitial lung diseases (ILD) is not clear. The aim of the study was to examine the effect of sera from ILD patients on angiogenesis induced by human mononuclear cells (MNC) in relation to IL-6, IL-8, IL-12, and TNF&#945; serum level. Serum samples were obtained from 68 patients with ILD (sarcoidosis &#8211; SAR 26 patients, avian fanciers&#8217; lung &#8211; AFP 13, idiopathic pulmonary fibrosis &#8211; IPF 13, histiocytosis &#8211; HIS 8, scleroderma &#8211; SCL 8) and from 14 healthy controls. In order to evaluate angiogenesis the Sidky and Auerbach leukocytes induced angiogenesis assay was performed. Cytokines in sera were evaluated by ELISA. Sera from AFL, SAR and IPF patients significantly stimulated angiogenic activity of MNC as compared with sera from healthy donors (p<0.001). However, sera from healthy subjects significantly stimulated angiogenic activity of MNC as compared with the control with PBS and with sera from HIS and SCL patients (p<0.001). The IL-12 serum level was significantly elevated in SAR patients compared with healthy controls and other groups. The TNF&#945; serum level was significantly elevated in HIS and SAR patients compared with healthy control and SCL patients. The highest IL-8 serum level was observed in sera from IPF patients and the lowest one in AFL patients (p<0.05). We have not found any correlation between proangiogenic properties simultaneously determined in sera and IL-6, IL-8 and IL-12 serum level. However, we observed a correlation between serum TNF&#945; level and the angiogenic activity of sera from ILD patients (p<0.05). Sera from ILD patients and healthy people constitute the source of mediators modulating angiogenesis but the pattern of reaction is different in various diseases. Sera from SCL and HIS patients exert an inhibitory effect on angiogenesis while sera from AFL, SAR and IPF patients stimulate neovascularisation. TNF&#945; as an important proinflammatory factor may stimulate angiogenesis in ILD.