IgE regulates mouse basophil Fc epsilon RI expression in vivo
Lantz, C.S.; Yamaguchi, M.; Oettgen, H.C.; Katona, I.M.; Miyajima, I.; Kinet, J.P.; Galli, S.J.
Journal of Immunology 158(6): 2517-2521
1997
ISSN/ISBN: 0022-1767 PMID: 9058781 Document Number: 480663
The binding of IgE to high affinity IgE receptors (Fc epsilon RI) on the surface of mast cells and basophils primes these cells to secrete a panel of proinflammatory mediators upon subsequent exposure to specific antigens. It was found that the level of Fc epsilon RI expression on bone marrow basophils in mice infected with Strongyloides venezuelensis exhibited a strong positive correlation with the serum concentration of IgE, as was previously reported for human blood basophils. Moreover, the in vivo administration of IgE significantly upregulated Fc epsilon RI expression on mouse basophils and genetically IgE-deficient (IgE -/-) mice exhibited a dramatic (~ 81%) reduction of basophil Fc epsilon RI expression compared with the corresponding normal (IgE +/+) mice. The finding that IgE can be a major regulator of mouse basophil Fc epsilon RI expression identified a potentially important mechanism for enhancing the expression of effector cell function in IgE-dependent allergic reactions or immunological responses to parasites.