Journal
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA
Volume 109, Issue 37, Pages 14954-14959Publisher
NATL ACAD SCIENCES
DOI: 10.1073/pnas.1117584109
Keywords
hematopoesis; Fc receptors; IgG1; IgE
Categories
Funding
- Swiss National Science Foundation [310030_133104]
- Health Research Council of New Zealand
- Marjorie Barclay Trust
- Swiss Vaccine Research Institute
- Swiss Federal Institute of Technology [TH-1507-3]
- Wellcome Trust
- Swiss National Science Foundation (SNF) [310030_133104] Funding Source: Swiss National Science Foundation (SNF)
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Basophils are powerful mediators of Th2 immunity and are present in increased numbers during allergic inflammation and helminth infection. Despite their ability to potentiate Th2 immunity the mechanisms regulating basophil development remain largely unknown. We have found a unique role for isotype-switched antibodies in promoting helminth-induced basophil production following infection of mice with Heligmosomoides polygyrus bakeri or Nippostrongylus brasiliensis. H. polygyrus bakeri-induced basophil expansion was found to occur within the bone marrow, and to a lesser extent the spleen, and was IL-3 dependent. IL-3 was largely produced by CD4(+)CD49b(+)NK1.1(-) effector T cells at these sites, and required the IL-4R alpha chain. However, antibody-deficient mice exhibited defective basophil mobilization despite intact T-cell IL-3 production, and supplementation of mice with immune serum could promote basophilia independently of required IL-4R alpha signaling. Helminth-induced eosinophilia was not affected by the deficiency in isotype-switched antibodies, suggesting a direct effect on basophils rather than through priming of Th2 responses. Although normal type 2 immunity occurred in the basopenic mice following primary infection with H. polygyrus bakeri, parasite rejection following challenge infection was impaired. These data reveal a role for isotype-switched antibodies in promoting basophil expansion and effector function following helminth infection.
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