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Endogenous Superallergen Protein Fv Induces IL-4 Secretion from Human FcRI⁺ Cells Through Interaction with the V_H3 Region of IgE¹

Vincenzo Patella^*, Ada Giuliano, Jean-Pierre Bouvet and Gianni Marone^2,*

^* Division of Clinical Immunology and Allergy, University of Naples Federico II, and Istituto Nazionale Tumori Giovanni Pascale, Naples, Italy; and Unité d’Immunopathologie Humaine, Institut National de la Santé et de la Recherche Médicale U430, Hôpital Broussais, Paris, France

We investigated the mechanism whereby protein Fv (pFv), a human sialoprotein found in normal liver and largely released in the intestinal tract in patients with viral hepatitis, induces mediator release from basophils and mast cells and evaluated whether it also induces IL-4 synthesis and secretion in basophils. pFv is a potent stimulus for histamine and IL-4 release from purified basophils. Histamine and IL-4 secretion from basophils activated by pFv was significantly correlated (r_s = 0.70; p < 0.001). There was also a correlation (r_s = 0.58; p < 0.01) between the maximum pFv- and anti-IgE-induced IL-4 release from basophils. The average t_1/2 for pFv-induced histamine release was lower (3.5 ± 1.5 min) than for IL-4 release (79.5 ± 8.5 min; p < 0.01). IL-4 mRNA, constitutively present in basophils, was increased after stimulation by pFv and was inhibited by cyclosporin A and tacrolimus. Basophils from which IgE had been dissociated by brief exposure to lactic acid no longer released IL-4 in response to pFv and anti-IgE. The response to an mAb cross-linking the -chain of FcRI was unaffected by this treatment. Three human V_H3⁺ monoclonal IgM concentration-dependently inhibited pFv-induced secretion of IL-4 and histamine from basophils and of histamine from human lung mast cells. In contrast, V_H6⁺ monoclonal IgM did not inhibit the release of IL-4 and histamine induced by pFv. These results indicate that pFv, which acts as an endogenous superallergen, interacts with the V_H3 domain of IgE to induce the synthesis and release of IL-4 from human FcRI⁺ cells.

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