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Airway IgG Counteracts Specific and Bystander Allergen-Triggered Pulmonary Inflammation by a Mechanism Dependent on FcR and IFN-¹

Sarita Sehra^*, Gwenda Pynaert^*, Kurt Tournoy, Anuschka Haegeman^*, Patrick Matthys, Yohichi Tagawa, Romain Pauwels and Johan Grooten^2,*

^* Department for Molecular Biomedical Research, Unit of Molecular Immunology, Flanders Interuniversity Institute for Biotechnology and Ghent University, Ghent, Belgium; Department of Respiratory Diseases, Ghent University, Ghent, Belgium; Laboratory of Immunobiology, Rega Institute for Medical Research, University of Leuven, Leuven, Belgium; and Institute of Experimental Animals, Shinshu University School of Medicine, Nagano, Japan

Besides IgE, the Ab isotype that gives rise to sensitization and allergic asthma, the immune response to common inhalant allergens also includes IgG. Increased serum titers of allergen-specific IgG, induced spontaneously or by allergen vaccination, have been implicated in protection against asthma. To verify the interference of topical IgG with the allergen-triggered eosinophilic airway inflammation that underlies asthma, sensitized mice were treated by intranasal instillation of specific IgG, followed by allergen challenge. This treatment strongly reduced eosinophilic inflammation and goblet cell metaplasia, and increased Th1 reactivity and IFN- levels in bronchoalveolar lavage fluid. In contrast, inflammatory responses were unaffected in IFN--deficient mice or when applying F(ab')₂. Although dependent on specific allergen-IgG interaction, inflammation triggered by bystander allergens was similarly repressed. Perseverance of inflammation repression, apparent after secondary allergen challenge, and increased allergen capture by alveolar macrophages further characterized the consequences of topical IgG application. These results assign a novel protective function to anti-allergen IgG namely at the local level interference with the inflammatory cascade, resulting in repression of allergic inflammation through an FcR- and IFN--dependent mechanism. Furthermore, these results provide a basis for topical immunotherapy of asthma by direct delivery of anti-allergen IgG to the airways.

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