T cell-derived IL-3 plays key role in parasite infection-induced basophil production but is dispensable for in vivo basophil survival

Tao Shen, Sohee Kim, Jeong Su Do, Lu Wang, Chris Lantz, Joseph F. Urban, Graham Le Gros, Booki Min*

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

70 Scopus citations

Abstract

Enhanced basophil production is often associated with Th 2-related conditions such as parasite infections or allergic inflammations. Our previous study demonstrated that T cell activation is necessary to promote basophil production in Nippostrongylus brasiliensis (Nb)-infected mice. Yet, mechanisms underlying how T cells aid infection-induced basophil production are not clear. In this report, we show that IL-3 produced by T cells activated by the infection enhances basophil production in Nb-infected mice. IL-3-deficient mice or Rag2-/- recipients of IL-3-deficient T cells but not of wild-type T cells failed to support basophil production following the Nb infection. Interestingly, although IL-3 was critical for preventing basophil apoptosis in vitro, IL-3 had little contribution to basophil survival and proliferation in vivo. Collectively, these results highlight a novel mechanism by which activation of adaptive immune components induces basophil production but not basophil survival via IL-3 production.

Original languageEnglish (US)
Pages (from-to)1201-1209
Number of pages9
JournalInternational Immunology
Volume20
Issue number9
DOIs
StatePublished - 2008
Externally publishedYes

Keywords

  • Apoptosis
  • Basophils
  • IL-3
  • Parasitic helminth

ASJC Scopus subject areas

  • Immunology and Allergy
  • Immunology

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