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© Matteo Bonazzi, Edith Gouin
Observation en immunofluorescence d'une cellule infectée par Listeria monocytogenes. En bleu: marquage des protéines de surface de Listeria qui permet de visualiser les bactéries. En rouge et vert: marquage de l'actine, une protéine qui forme le cytosquelette des cellules. Les Listeria utilisent l'actine cellulaire pour former des "comêtes" et se déplacer à l'intérieur des cellules qu'elles infectent. Cell infected by Listeria monocytogenes. The surface proteins (in blue) of Listeria enable us to view the bacteria. Actin, a constituent protein of cells, is shown in red and green.
Publication : Journal of immunology (Baltimore, Md. : 1950)

Cutting edge: intravenous Ig inhibits invariant NKT cell-mediated allergic airway inflammation through FcγRIIIA-dependent mechanisms

Team: Antibodies in Therapy and Pathology
Scientific Fields
Diseases
Organisms
Applications
Technique

Published in Journal of immunology (Baltimore, Md. : 1950) - 11 Feb 2011

Araujo LM, Chauvineau A, Zhu R, Diem S, Bourgeois EA, Levescot A, Huerre M, Gombert JM, Bayry J, Daëron M, Bruhns P, Kaveri SV, Herbelin A

Link to Pubmed [PMID] – 21317388

J. Immunol. 2011 Mar;186(6):3289-93

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 FcγRIIIA, 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 α-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 FcγRIIIA(-/-) mice. Our data unravel an FcγRIIIA-dependent inhibitory effect of IVIg on activated iNKT cells that confers protection in AAI.