| First Author | Blink SE | Year | 2010 |
| Journal | Cell Immunol | Volume | 264 |
| Issue | 1 | Pages | 54-60 |
| PubMed ID | 20494341 | Mgi Jnum | J:162109 |
| Mgi Id | MGI:4462756 | Doi | 10.1016/j.cellimm.2010.04.011 |
| Citation | Blink SE, et al. (2010) IgE regulates T helper cell differentiation through FcgammaRIII mediated dendritic cell cytokine modulation. Cell Immunol 264(1):54-60 |
| abstractText | 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 FcgammaRIII 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 FcgammaRIII on dendritic cells. |
