Inhibition of the anti-receptor antibody response of contact sensitivity by interferon

Mice sensitized with optimal doses of 2,4-dinitrofluorobenzene (DNFB) develop maximum delayed hypersensitivity in 4-5 days; the intensity of this reaction declines rapidly 14 days after sensitization. In the serum of mice 14 days after sensitization, an anti-receptor antibody has been described. It has been suggested that this antibody might be responsible for this rapid decline of contact sensitivity. We studied the effect of interferon alpha, beta (IFN alpha, beta) and cyclophosphamide (Cy) in this model. IFN alpha, beta (2 X 10(4) units/ mouse) or Cy (200 mg/kg) injected at Days 0 and 1 during sensitization, or at Day -2 before sensitization, respectively, partially prevented the decline of contact sensitivity as compared to the controls. In the serum of mice treated with IFN or Cy, no anti-receptor antibody could be detected 14 days after sensitization. These results suggest that anti-receptor antibody may be partially responsible for the waning of contact sensitivity. It is further suggested that IFN inhibited the anti-receptor antibody response by preventing the generation of the anti-receptor-antibody-inducing auxiliar T-suppressor cell. It is concluded that IFN alpha, beta enhances the delayed hypersensitivity response in contact allergy by inhibition of the T-suppressor circuit, as previously reported, and by suppression of the anti-receptor antibody response.