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Signaling through FcRIII is required for optimal T helper type (Th)2 responses and Th2-mediated airway inflammation

¹ Committee on Immunology and ² Section of Pulmonary and Critical Care Medicine, Department of Medicine, University of Chicago, Chicago, IL 60637
³ Department of Human Genetics, Leiden University Medical Center, 2300 RC Leiden, Netherlands
⁴ Department of Internal Medicine, Tufts University, Boston, MA 02111

CORRESPONDENCE Anne I. Sperling: asperlin{at}uchicago.edu

Although inhibitory Fc receptors have been demonstrated to promote mucosal tolerance, the role of activating Fc receptors in modulating T helper type (Th)2-dependent inflammatory responses characteristic of asthma and allergies remains unclear. Here, we demonstrate that signaling via activating Fc receptors in conjunction with Toll-like receptor 4 stimulation modulated cytokine production from bone marrow–derived dendritic cells (DCs) and augmented their ability to promote Th2 responses. Ligation of the low affinity receptor FcRIII was specifically required for the enhanced Th2 responses, as FcRIII^–/– DCs failed to augment Th2-mediated airway inflammation in vivo or induce Th2 differentiation in vitro. Further, FcRIII^–/– mice had impaired Th2 cytokine production and exhibited reduced airway inflammation, whereas no defect was found in FcRI^–/– mice. The augmentation of Th2 immunity was regulated by interleukin 10 production from the DCs but was distinct and independent of the well-established role of FcRIII in augmenting antigen presentation. Thus, our studies reveal a novel and specific role for FcRIII signaling in the regulation of Th cell responses and suggest that in addition to immunoglobulin (Ig)E, antigen-specific IgG also contributes to the pathogenesis of Th2-mediated diseases such as asthma and allergies.

H.S. Bandukwala and B.S. Clay contributed equally to this work.

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