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International Immunology Advance Access published online on July 15, 2008
International Immunology, doi:10.1093/intimm/dxn077
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© The Japanese Society for Immunology. 2008. All rights reserved. For permissions, please e-mail: journals.permissions@oxfordjournals.org

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

Tao Shen1, Sohee Kim1, Jeong-su Do1, Lu Wang1, Chris Lantz2, Joseph F. Urban3, Graham Le Gros4 and Booki Min1

1 Department of Immunology/NB30, Lerner Research Institute, Cleveland Clinic Foundation, 9500 Euclid Avenue, Cleveland, OH 44195, USA
2 Department of Biology, James Madison University, Harrisonburg, VA 22807, USA
3 Diet, Genomics and Immunology Laboratory, United States Department of Agriculture, Beltsville, MD 20705, USA
4 Malaghan Institute of Medical Research, Wellington, New Zealand

Correspondence to: Correspondence to: B. Min; E-mail: minb{at}ccf.org

Enhanced basophil production is often associated with Th2-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.

Keywords: apoptosis, basophils, IL-3, parasitic helminth

Transmitting editor: S. Galli

Received 30 October 2007, accepted 11 June 2008.


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