title: Defective B-1 cell development and impaired immunity against Angiostrongylus cantonensis in IL-5R alpha-deficient mice.
abstract: We generated interleukin-5 receptor alpha chain (IL-5R alpha)-deficient (IL-5R alpha-/-) mice by gene targeting. The IL-5R alpha-/- mice showed decreased numbers of B-1 cells concomitant with low serum concentrations of IgM and IgG3. They showed no IL-5-induced enhancement of B cell responses to T-independent antigens. The number of alpha beta T cell receptor-positive thymocytes tended to decrease in 3-week-old IL-5R alpha-/- mice, returning to normal by 6 weeks of age. The IL-5R alpha-/- mice produced basal levels of eosinophils, while their bone marrow cells failed to form eosinophilic colonies in response to IL-5. Impaired eosinophilopoiesis in IL-5R alpha-/-mice enhanced the survival of Angiostrongylus cantonensis. These results indicate that IL-5-induced eosinophils serve as potent effector cells in the killing of Angiostrongylus cantonensis in mice.
authors.affiliation: Department of Immunology, Faculty of Medicine, University of Tokyo, Japan.
authors.forename: T
authors.initials: T
authors.lastname: Yoshida
authors.forename: K
authors.initials: K
authors.lastname: Ikuta
authors.forename: H
authors.initials: H
authors.lastname: Sugaya
authors.forename: K
authors.initials: K
authors.lastname: Maki
authors.forename: M
authors.initials: M
authors.lastname: Takagi
authors.forename: H
authors.initials: H
authors.lastname: Kanazawa
authors.forename: S
authors.initials: S
authors.lastname: Sunaga
authors.forename: T
authors.initials: T
authors.lastname: Kinashi
authors.forename: K
authors.initials: K
authors.lastname: Yoshimura
authors.forename: J
authors.initials: J
authors.lastname: Miyazaki
authors.forename: S
authors.initials: S
authors.lastname: Takaki
authors.forename: K
authors.initials: K
authors.lastname: Takatsu
mesh_terms: D017185:Angiostrongylus cantonensis / Q000254:growth & development / Q000276:immunology*; D000818:Animals; D001402:B-Lymphocytes / Q000276:immunology / Q000378:metabolism / Q000473:pathology*; D001927:Brain Diseases / Q000235:genetics / Q000276:immunology / Q000469:parasitology; D002454:Cell Differentiation / Q000276:immunology; D004804:Eosinophils / Q000473:pathology; D006410:Hematopoiesis / Q000276:immunology; D017099:IgG Deficiency / Q000235:genetics; D007075:Immunoglobulin M / Q000172:deficiency; D015848:Interleukin-5 / Q000378:metabolism* / Q000627:therapeutic use; D008231:Lymphopenia / Q000235:genetics / Q000276:immunology; D051379:Mice; D008817:Mice, Mutant Strains; D018123:Receptors, Interleukin / Q000172:deficiency* / Q000235:genetics* / Q000276:immunology; D053649:Receptors, Interleukin-5; D017206:Strongylida Infections / Q000134:cerebrospinal fluid / Q000235:genetics / Q000276:immunology*; D013601:T-Lymphocytes / Q000473:pathology
chemical_list: D007075:Immunoglobulin M; D015848:Interleukin-5; D018123:Receptors, Interleukin; D053649:Receptors, Interleukin-5