Allergy.
1995 Jun;15(2):205-215.
Regulation of IgE production in patients with atopic disease: Imbalance of IL - 4 and IFN - gamma production
Abstract
- IgE antibodies play a major role in the development of atopic disease because they bind to high affinity receptors on mast cells and basophiis and when cross linked by allergen cause cellular degranulation with the release of vaso active amines. After discovery of IgE molecule by Ishizaka in 1966, there has been many studies about IgE synthesis and it's regulation. Recently, it has been demonstrated that IL-4 induce IgE synthesis in vitro from mononuclear cells isolated from peripheral blood, tonsils and spleens of healthy persons and IL-4-induced IgE synthesis is blocked by IFN-gamma. Spontaneous IgE synthesis in vitro from mononuclear cells of atopic patients is also higher than that from healthy persons.
There is evidence that IL-4 and IFN-gamma, are produced by different subsets of helper T cell, TH1 and TH2 cell. IL-4 is produced by TH2, while IFN-gamma is produced by TH1. The differences of IL 4 and IFN-gamma secretion by allergen and mitogen between atopic patients and healthy persons are not clear until now. To investigate the differences of IL-4 and IFN-gamma secretion by allergen and mitogen between atopic patients and healthy subjects, concentrations of IL-4 and IFN-gamma in the culture supernatants stimulated with and without mitogens and allergens were measured by ELISA method. The results are as follows: 1) IL-4 levels in culture supernatants of PBMNCs were increased by stimulation with PMA and calcium ionophore A 23187 and allergen in both group. In atopic patients activation of PBMNCs resulted in higher levels of II, 4 than those of healthy controls. 2) There was a significant correlation between IL-4 level in culture supernatant of PBMNCs stimulated with PMA and calciumionophore A 23187 and serum total IgE (r=0. 57, p<0.05). And there was a significant torrelation between IL-4/IFN-gamma ratio and serum total IgE (r=0.48, P< 0.05). 3) In atopic patients, activation of PBMNCs resulted in lower levels of IFN-gamma than those of healthy controls. There was no significant correlation between the levels of IFN-gamma in cultures supernatant stimulated with PMA and calciumionophore and serum total IgE(r=0.35, p>0.05). These results suggest that high levels of antibody in serum of atopic patients may be due to imbalance of IL-4 and IFN-gamma secreting capacities of atopic patients.