title: IgG and IgE collaboratively accelerate expulsion of Strongyloides venezuelensis in a primary infection.
abstract: The host deploys a subset of immune responses to expel helminths, which differs depending on the nature of the helminth. Strongyloides venezuelensis, a counterpart of the human pathogen S. stercoralis, naturally infects rodents and has been used as an experimental model. Here we show that induction of immunoglobulin G (IgG) and IgE is a prerequisite for rapid expulsion of S. venezuelensis during a primary infection. Activation-induced cytidine deaminase-deficient (AID(-/-)) mice, which lack the ability to switch IgM to other isotypes, normally developed T-helper 2 (Th2) cells and intestinal mastocytosis after infection with S. venezuelensis. Although AID(-/-) mice expelled Nippostrongylus brasiliensis normally, they required a much longer period to expel S. venezuelensis than wild-type (WT) mice. Adoptive transfers of immune sera from S. venezuelensis-infected but not N. brasiliensis-infected mice restored the ability of AID(-/-) mice to promptly expel S. venezuelensis. Immune serum-derived IgG and IgE induced worm expulsion via Fc γ receptor III (FcγRIII) and Fc ε receptor I (FcεRI), respectively, and a mixture of IgG and IgE showed collaborative effects. Whereas FcγRIII(-/-) mice or FcεRIα(-/-) mice normally could expel S. venezuelensis, FcγRIII(-/-) mice, when their IgE was neutralized by anti-IgE, or FcεRIα(-/-) mice, when their IgG binding to FcγRIII was blocked by anti-FcγRIII, showed a markedly reduced ability to expel S. venezuelensis. These data reveal that IgG and IgE play redundant roles but act in concert to accelerate S. venezuelensis expulsion. Mast cell-deficient mice, even those equipped with immune serum-derived IgG or IgE, failed to expel S. venezuelensis promptly, suggesting that mast cells are cellular targets of IgG and IgE.
authors: Department of Immunology and Medical Zoology, Hyogo College of Medicine, Nishinomiya, Japan.
authors: Makoto
authors: M
authors: Matsumoto
authors: Yuki
authors: Y
authors: Sasaki
authors: Koubun
authors: K
authors: Yasuda
authors: Toshiyuki
authors: T
authors: Takai
authors: Masamichi
authors: M
authors: Muramatsu
authors: Tomohiro
authors: T
authors: Yoshimoto
authors: Kenji
authors: K
authors: Nakanishi
mesh_terms: D000818:Animals; D049109:Cell Proliferation; D007116:Immunization, Passive; D017578:Immunoglobulin Class Switching; D007073:Immunoglobulin E / Q000008:administration & dosage / Q000276:immunology*; D007074:Immunoglobulin G / Q000008:administration & dosage / Q000276:immunology*; D008407:Mast Cells / Q000276:immunology / Q000469:parasitology; D051379:Mice; D008810:Mice, Inbred C57BL; D018345:Mice, Knockout; D009559:Nippostrongylus / Q000276:immunology; D011485:Protein Binding; D051381:Rats; D017207:Rats, Sprague-Dawley; D017208:Rats, Wistar; D017455:Receptors, IgE / Q000276:immunology; D017452:Receptors, IgG / Q000276:immunology; D017206:Strongylida Infections / Q000276:immunology; D013321:Strongyloides / Q000276:immunology*; D013322:Strongyloidiasis / Q000276:immunology* / Q000517:prevention & control; D018418:Th2 Cells / Q000276:immunology
chemical_list: C579617:FcepsilonRIalpha protein, mouse; C485700:Fcgr3 protein, mouse; D007074:Immunoglobulin G; D017455:Receptors, IgE; D017452:Receptors, IgG; D007073:Immunoglobulin E
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