Abstract Two groups of patients suffering from interstitial lung diseases (ILD) namely sarcoidosis (SA) and idiopathic pulmonary fibrosis (IPF) were investigated for alveolar macrophages (AM), secretion of prostaglandin E 2 (PGE 2) and interleukin 1 (IL-1), together with superoxide anion (O 2 −) production. Peripheral blood monocytes (PBMO) of the same patients were examined concomitantly for suppressive activity. Consistent with previous results, AM obtained by bronchoalveolar lavage (BAL) from ILD patients markedly suppressed the effects of PHA stimulation of autologous peripheral blood lymphocytes (APL): 61.8 ± 9.7% suppressive activity compared to 15.5 ± 15.4% in the control group (CO) P<0.001. The AM suppressive activity was correlated with an increase in PGE 2 secretion: 3.861 ± 2.194 ng/10 5 cells/ml in the IPF group, but not in the sarcoid group: 0.217 ± 0.116 ng/10 5 cells/ml ( P<0.001 between them). On the other hand, IL-1 secretion by AM was greatly increased in sarcoid patients (308 ± 196 U/ml) but was within the normal limits in IPF (27.3 ± 28.8 U/ml, P<0.01 between them). Therefore, an inverse correlation was found between degree of PGE 2 secretion and IL-1 release by AM in ILD. O 2 − production by AM was markedly increased in all ILD patients but this mechanism is apparently not involved in suppressive activity. PBMO originating from ILD patients were less suppressive than the corresponding AM.