Background: Allergic inflammation may be the basis of bronchial hyperresponsiveness that is a characteristic of bronchial asthma. Lymphocytes are prominent among the inflammatory cells infiltrating asthmatic airways and express low affinity IgE receptor. We performed this study to evaluate the role of T- lymphocyte in the development of bronchial asthma. Methods: We measured delayed skin responsiveness to multiple recall antigens, lymphocyte blastogenesis to mitogens and allergen and surface markers of Tl-ymphocyte such as CD3, CD4, CD8, IL-2R, HLA-DR, VLA-1 by flowcytometric technique in 30 allergic asthmatics, 12 patients who showed improvement with immunotherapy and 11 healthy subjects. Results: 1) IL-2R(+) cells and HLA-DR(+) cells were in- creased significantly compared to those of controls (IL-2R(+) cells were 9.9±4.9%, 3.7±1.8%; HLA-DR(+) cells were 9.9±5.2%, 3.7±3% respectively). And IL-2R(+) cells showed inverse relationship with bronchial hyperresponsiveness. CD8(+) cells were increased in asthmatics, but CD3(+) cells and CD4(+) cells were not different from those of controls. Cell surface markers were not changed with immunotherapy. 2) Lymphoproliferative responses to PHA(10-100 ug/ml), Con A(1-10 ug/m1) and D.farinae (10-6-10-2 w/v%) showed no significant differences among D.farinae sensitive asthmatics, immunotherapy patients and healthy controls. 3) Delayed skin responses to multiple recall antigens were similar among groups. 4) None of lymphoproliferative responses, cell surface markers and delayed skin responses of allergic asthmatics showed significant correlation with parameters of type 1 hypersensitivity reaction. Conclusion: CD8(+) cells are increased in allergic asthmatics, and the lymphoproliferative responses to allergens and mitogens are not changed compared to healthy controls. And activated Tlymphocytes play an important role in the development of allergic asthma.