Regulation of Contact Allergy by Interferon

Abstract

Interferon (α, β and γ) has multiple effects on the immune system and it seems most likely that it is an important immune regulatory molecule. Original observations using experimental contact allergy models have shown that high doses of interferon α, β can suppress or enhance contact sensitivity in vivo, depending on the time of administration in relation to the sensitizing application of the contact sensitizer. We have observed that interferon released by C. parvum treatment of BALB/c mice enhanced contact sensitivity to 2,4-dinitrofluorobenzene (DNFB) and further analysis of this phenomenon showed that interferon α, β and γ in very low doses blocked the T suppressor pathway of this delayed type hypersensitivity reaction. We further tried to analyze the mechanism of this interferon-mediated blockade of the T suppressor pathway, using an in vitro model of contact sensitivity. From the observation obtained in this model we concluded that interferon blocked the T suppressor lymphocyte directly and not via antigen-presenting macrophages. It was further shown that antigen-presenting macrophages particularly able to activate T suppressor cells produced much less interferon than those able to activate T effector lymphocytes. Adding antiinterferon globulin to cultures containing macrophages able to induce T effector cells but unable to activate T suppressor cells resulted in an activation of T suppressor lymphocytes; this indicates that the ability of macrophage populations to produce interferon could be related to the ability to activate T effector or T suppressor lymphocytes.