Reduced priming effect of interleukin 3 on IgE mediated basophil histamine release in patients with systemic sclerosis.

Abstract

To determine the capacity of interleukin 3 (IL-3) to induce and enhance basophil histamine release in patients with systemic sclerosis (SSc). Leukocyte suspensions prepared by dextran sedimentation of peripheral venous blood were stimulated with anti-IgE (10 microg/ml), N-formyl-methionyl-leucyl-phenylalanine (fMLP, 1 microM), and IL-3 (0.1 to 10 ng/ml). The priming effect of IL-3 on anti-IgE and fMLP induced histamine release was evaluated. Histamine release was measured by an automated fluorometric method. No significant difference was found between patients with SSc (n = 12) and control subjects (n = 16) regarding spontaneous IL-3 and fMLP induced histamine release. IL-3 was a weak basophil agonist in both populations, since net histamine release did not exceed 10% of total histamine content in any case. Anti-IgE induced histamine release was lower in patients with SSc than in controls (13.09 +/- 4.8 vs 30.2 +/- 6.2%; p = 0.048). IL-3 enhanced anti-IgE and fMLP induced histamine release in a dose dependent fashion. However, the enhancement of anti-IgE induced histamine release by IL-3 was significantly lower in patients with SSc than in controls (p < 0.01 at 0.1 ng/ml IL-3; p < 0.05 at 1 and 10 ng/ml IL-3). In contrast, no difference was found between the 2 populations regarding the enhancement of fMLP induced histamine release by IL-3. Basophil response to anti-IgE and the priming effect of IL-3 on IgE mediated basophil histamine release are lower in patients with SSc than in controls. These alterations could be related to chronic activation of the IgE/basophil system in patients with SSc.