| First Author | Araujo LM | Year | 2011 |
| Journal | J Immunol | Volume | 186 |
| Issue | 6 | Pages | 3289-93 |
| PubMed ID | 21317388 | Mgi Jnum | J:169761 |
| Mgi Id | MGI:4942214 | Doi | 10.4049/jimmunol.1003076 |
| Citation | Araujo LM, et al. (2011) Cutting Edge: Intravenous Ig Inhibits Invariant NKT Cell-Mediated Allergic Airway Inflammation through Fc{gamma}RIIIA-Dependent Mechanisms. J Immunol 186(6):3289-93 |
| abstractText | Despite their increasing use in autoimmune, inflammatory, and allergic conditions, the mechanism of action of i.v. Igs (IVIg) is poorly understood. On the basis of the critical role of invariant NKT (iNKT) cells in allergic airway inflammation (AAI) and their constitutive expression of the low-affinity IgG receptor FcgammaRIIIA, we surmised that IVIg targets iNKT cells to exert their anti-inflammatory effect. We found that IVIg treatment significantly inhibited AAI in OVA-sensitized C57BL/6 mice and downregulated alpha-galactosylceramide-induced iNKT cell activation and cytokine production. Allergic responses were restored in iNKT cell-deficient mice by transferring iNKT cells from PBS- but not from IVIg-treated mice, suggesting that IVIg acts directly on activated iNKT cells that have a critical role in AAI. The inhibitory effects of IVIg on both iNKT cell activation/function and OVA-driven AAI were lost in FcgammaRIIIA(-/-) mice. Our data unravel an FcgammaRIIIA-dependent inhibitory effect of IVIg on activated iNKT cells that confers protection in AAI. |
