We have experienced a patient with intractable mycosis fungoides (MF) who has been treated successfully with recombinant human interferon-γ (IFN-γ) for a period of 7 and half years. This therapy was shown to be a safe alternative to other medications with unacceptable side effects and decreasing the dosage of IFN-γ should be done very slowly in order to maintain complete remission.
In the early stages of disease, T-and B-cell responses are usually unaltered. However, as the disease progresses, T-cell responses to antigens and mitogens, NK cell activity, lymphokine-activated killer cell (LAK) activity, are known to decrease in association with an increase in levels of immunoglobulins IgE and IgA. Recently the peripheral blood cells of patients with MF were shown to exhibit abnormal production of IL-4, as well as a defect in INF-γ release. IL-4 can antagonize the biological activity of INF-γ and can inhibit the production of this cytokine. This lymphokine secretion pattern may help explain the observed immunologic abnormalities present in advanced disease. Interestingly, IFN-γ antagonizes the biologic activity or IL-4. Thus in the initial stages of MF, IL-4 and IFN-γ may be counteracting a portion of each other's activity. Since the reintroduction of IFN-γ exogenously could patially inhibit the enhanced production of IL-4, leading ultimately to augmented NK cell activity and decreased proliferation of tumor cells, thus, the use of IFN-γ may offer therapeutic benefits to patients with MF.
Natural killer cell stimuratory factor (IL-12) is known to induce IFN-γ production by T and NK cells. IL-10 efficiently inhibits a IL-12 production, leading to the decrease in IFN-γ. The reciprocal regulation of these cytokines may result in the abnormal regulation of cellular and humoral immune response in MF. The elucidation of these cytokine interactions will provide highly specific immunotherapeutic approaches to MF.