IgE regulates T helper cell differentiation through FcI[sup3RIII mediated dendritic cell cytokine modulation

• Published in: Cellular immunology Vol. 264; no. 1; pp. 54 - 60
• Main Authors: Blink, Sarah E, Fu, Yang-Xin
• Format: Journal Article
• Language: English
• Published: 01.01.2010
• Subjects: Asthma
• ISSN: 0008-8749
• DOI: 10.1016/j.cellimm.2010.04.011

Asthma and allergy are characterized by dysregulation of inflammatory responses toward Th2 responses and high serum levels of IgE. IgE plays a role in the effector phase by triggering the degranulation of mast cells after antigen-crosslinking but its role in the induction of helper T cell differentiation is unknown. We have previously shown lymphotoxin is required for maintaining physiological levels of serum IgE which minimize spontaneous Th1-mediated airway inflammation, suggesting a physiological role for IgE in the regulation of T helper cell differentiation. We describe the mechanism in which IgE modulates inflammation by regulating dendritic cell cytokine production. Physiological levels of IgE suppress IL-12 production in the spleen and lung, suggesting IgE limits Th1 responses in vivo. IgE directly stimulates dendritic cells through FcI[sup3RIII to suppress IL-12 in vitro and influences APC to skew CD4+ T cells toward Th2 differentiation. We demonstrate a novel role for IgE in regulating differentiation of adaptive inflammatory responses through direct interaction with FcI[sup3RIII on dendritic cells.