T-cell/eosinophil interactions in the induction of asthma.
There now exists considerable support for the hypothesis that asthma represents a specialized form of cell-mediated immunity, in which cytokines and possibly other mediators secreted by activated T-lymphocytes bring about the specific accumulation and activation of eosinophils in the bronchial mucosa. This observation has very important implications for future asthma therapy, since it suggests that drugs other than glucocorticoids which inhibit T-lymphocyte function may be of therapeutic benefit, as has recently been shown in the case of cyclosporin A. Further documentation of the cytokines involved in asthma of varying clinical associations might allow a pathophysiological classification of the disease.
Corrigan
C J
CJ
Dept of Medicine, Charing Cross and Westminster Medical School, University of London, UK.
Kay
A B
AB
D001249:Asthma / Q000188:drug therapy / Q000276:immunology*; D015496:CD4-Positive T-Lymphocytes / Q000276:immunology; D002450:Cell Communication / Q000276:immunology*; D002465:Cell Movement; D018925:Chemokines / Q000276:immunology; D016572:Cyclosporine / Q000627:therapeutic use; D004804:Eosinophils / Q000276:immunology*; D005938:Glucocorticoids / Q000627:therapeutic use; D006133:Growth Substances / Q000276:immunology; D006801:Humans; D007165:Immunosuppression Therapy; D007166:Immunosuppressive Agents / Q000627:therapeutic use; D007378:Interleukins / Q000276:immunology; D008168:Lung / Q000276:immunology; D015846:Monokines / Q000276:immunology; D013601:T-Lymphocytes / Q000276:immunology*; D018418:Th2 Cells / Q000276:immunology
D018925:Chemokines; D005938:Glucocorticoids; D006133:Growth Substances; D007166:Immunosuppressive Agents; D007378:Interleukins; D015846:Monokines; D016572:Cyclosporine