Modulation of Cytokine Production During Immunotherapy in Atopic Asthmatics: A Potential Role for Cytokine Antagonists. A Preliminary Study

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Background The pathogenesis of asthma involves hyperreactivity and chronic inflammation of airways in which CD4+ T cells play a major role. In atopic asthmatics, Thl responses due to interferon-gamma (IFN-γ) are depressed, and Th2 responses due to interleukins (IL-4, IL-10) are predominant. It is not clear if cytokine secretion patterns change with clinical improvement during immunotherapy. Objectives Monitoring IFN-γ and IL-10 may be very useful in evaluating the effectiveness and response to allergen immunotherapy and in developing new therapeutic interventions with specific cytokine antagonists or peptides. Materials and Methods Peripheral blood mononuclear cells were obtained from healthy nonasthmatic controls (N = 5) and from atopic asthmatic patients (N = 5) prior to immunotherapy and at 3 and 6 months after initiation of immunotherapy to monitor cytokine secretion (IFN-γ, IL-10) in unstimulated and grass and ragweed allergen-specific stimulated mononuclear cells. Changes in cytokine secretions were related to clinical response to immunotherapy. Results Controls had significantly higher mean IFN-γ secretion compared to asthmatics (P < 0.01). Mean IL-10 secretion was lower in controls than in asthmatics, but significant levels were noted only with grass allergen (P < 0.03). In asthmatics, 3 months after starting immunotherapy mean IFN-γ secretion significantly increased (P < 0.01) in both stimulated and unstimulated cells, which persisted at 6 months. Although there was no significant change in IL-10 secretion at 3 months, mean IL-10 secretion at 6 months was significantly decreased in allergen-stimulated cells (P < 0.02). Conclusion In atopic asthmatics, mean IFN-γ secretion significantly increased and allergen-specific IL-10 secretion was significantly decreased during immunotherapy.