We previously demonstrated that, in C57B1/6 mice, cyclosporin A enhanced and dexamethasone inhibited the Aspergillus fumigatus‐induced pulmonary eosinophilia and total IgE levels. To evaluate whether these effects were related to the modulation of T‐lymphocyte recruitment and activation and cytokine expression, we performed immunohistochemical staining for T‐cell surface marker CD3 and CD4, cell activation marker CD25, and cytokines granulocyte–macrophage colony‐stimulating factor (GM‐CSF), interleukin‐4 (IL‐4) and interleukin‐5 (IL‐5) on lung tissue sections from mice exposed to Aspergillus fumigatus and treated or not with dexamethasone or cyclosporin A. Dexamethasone significantly inhibited Aspergillus fumigatus‐induced increased number of activated T cells and cytokine‐expressing cells in parallel with a decrease in pulmonary eosinophils. In contrast, cyclosporin A did not decrease these immunological events but enhanced the lung eosinophil recruitment. Moreover, dexamethasone prevented the production of immunoglobulins against 76 and 36 kD antigen proteins and cyclosporin A against 76 and 18 kD antigen proteins. These results indicate that dexamethasone down‐regulates and cyclosporin A up‐regulates lung eosinophil recruitment and total IgE production, probably via the modulation of T‐lymphocyte activation and GM‐CSF, IL‐4 and IL‐5 expression. Both drugs inhibit Aspergillus fumigatus‐specific antibody synthesis, but their suppressive actions are selective to different antigenic components.