Inflammation in asthma is characterized by a Th2 response. In many experimental systems, this response can be regulated by interleukin (IL)‐IO and IL‐12. IL‐10 deactivates T cells, and IL‐12 reorients the response toward a Till pattern. Alveolar macrophages (AM) can secrete both of these cytokines, and thus regulate T‐cell behavior in asthma. They can enhance the Tli2 response by turning off their secretion of IL‐10 and IL‐12. or tend to downregulate it by producing these cytokines. To elucidate that point, we assayed the AM IL‐10 and IL‐12 from 11 asthmatic patients and four controls. Six asthmatics were treated by inhaled corticosteroids. AM were recovered by bronchoalveolar lavage (BAL). They were isolated and cultured for 24 h without stimulation or in the presence of lipopolysaccharide (LPS), IL‐10 and the p40 subunit of IL‐12 were assayed in the BAL fluid and i n AM culture supernatants by ELISA. Spontaneous AM IL‐10 production was higher in asthmatics, particularly in the treated group. The AM IL‐10 production after stimulation by LPS was also elevated in asthmatics, but was mainly so in untreated patients. IL‐12 levels were higher in BAL fluids from untreated patients than from controls. The IL‐12 production of LPS‐stitnulated‐AM from these patients was increased. These results show that AM are at least primed for the production of IL‐10 and IL‐12 in asthma, and suggest that these cells could be involved in the resolution of the asthmatic inflammation.