Proinflammatory cytokines, ie, tumor necrosis factor-alpha (TNFα), participate in the development and the progression of congestive heart failure (CHF). On the other hand, an anti-inflammatory cytokine may neutralize the proinflammatory cytokines of CHF. Interleukin-10 (IL-10) is known to suppress the synthesis of proinflammatory cytokines. IL-10 and the IL-10 receptor system was investigated in comparison with the behavior of TNF α in 68 patients with various causes of CHF (mean age: 61 years) and in 31 normal subjects (61 years). The circulating IL-10 level was higher in CHF patients than in normal subjects (p<0.05). The TNFα level was higher in CHF patients than in control subjects (p<0.005). The ratio of IL-10 to TNFα tended to be higher in control subjects than in patients with CHF (p=0.09). With lipopolysaccharide treatment, the release of IL-10 was more enhanced from mononuclear leukocyte of patients with CHF than from control subjects (p<0.05). The expression of the IL-10 receptor estimated by flow cytometry of mononuclear leukocytes was higher in the CHF patients than in the normal subjects. The IL-10/IL-10 receptor system was activated, at least partly, to downregulate an excess of TNF α in patients with advanced CHF. IL-10 may be an important inherent component of the cytokine network of CHF. (Jpn Circ J 1999; 63: 951 - 956)