Lack of Fc-ε receptors on murine eosinophils: Implications for the functional significance of elevated IgE and eosinophils in parasitic infections

Chronic infection with Schistosoma mansoni induces in humans and mice a Th2-dominant immune response in which eosinophils and IgE are conspicuously elevated. Human eosinophils express IgE receptors that participate in an IgE- dependent eosinophil-mediated ADCC reaction against Schistosomula larvae in vitro. To investigate the expression of IgE receptors on murine eosinophils, they were purified (>95% pure by Giemsa-stained cytospin preparations) from liver granulomas of Schistosoma-infected mice. Flow cytometric analysis showed the absence of the low-affinity IgE receptor Fc-ε RII (CD23) and Mac- 2 and the absence of binding of murine IgE. Reverse transcription-polymerase chain reaction (RT-PCR) analysis of granuloma eosinophil mRNA did not detect transcripts for FC-ε RII or the α-chain of the high-affinity IgE receptor Fc-ε RI, but did detect transcripts that encode Mac-2 and the low-affinity IgG receptors Fc-γ, RIIb2, Fc-γ RIII, and the FcR-associated γ-chain. In vitro stimulation of granuloma eosinophils with interleukin-4 (IL4) did not induce IgE binding, surface expression of Mac-2, or the transcription of Fc- ε receptors (Fc-ε RI, Fc-ε RII/CD23). To investigate normal murine eosinophils, we cultured normal mouse bone marrow cells with recombinant IL- 3, recombinant IL-5, and recombinant granulocyte-macrophage colony- stimulating factor, conditions that promote eosinophil differentiation. Flow cytometric analysis of bone marrow derived eosinophils failed to detect IgE binding or cell surface expression of Fc-ε RII and Mac-2, and RT-PCR analysis of fluorescence-activated cell sorted bone marrow-derived eosinophils failed to detect transcripts that encode Fc-ε RI or Fc-ε RII. These findings show that, in contrast to human eosinophils, murine eosinophils do not express cell surface receptors that bind IgE. However, because IgG receptors (Fc-γ RIIb2, Fc-γ RIII) were present on eosinophils purified from granulomas, we investigated whether they might be involved in eosinophil activation. We found that an oxidative burst in eosinophils could be triggered through their IgG receptors.