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

Int Immunol. 2008 Sep;20(9):1201-9. doi: 10.1093/intimm/dxn077. Epub 2008 Jul 15.


Enhanced basophil production is often associated with T(h)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.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Apoptosis
  • Basophils / immunology*
  • Basophils / physiology
  • Interleukin-3 / immunology
  • Interleukin-3 / metabolism*
  • Lymphocyte Activation / immunology*
  • Mice
  • Mice, Inbred BALB C
  • Mice, Inbred C57BL
  • Nippostrongylus / pathogenicity*
  • Strongylida Infections / immunology*
  • Strongylida Infections / parasitology
  • T-Lymphocytes / immunology*
  • T-Lymphocytes / metabolism


  • Interleukin-3