International Immunology Advance Access originally published online on July 15, 2008
International Immunology 2008 20(9):1201-1209; doi:10.1093/intimm/dxn077
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
T cell-derived IL-3 plays key role in parasite infection-induced basophil production but is dispensable for in vivo basophil survival
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: 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.
![]()
CiteULike
Connotea
Del.icio.us What's this?
This article has been cited by other articles:
![]() |
E. Kuroda, V. Ho, J. Ruschmann, F. Antignano, M. Hamilton, M. J. Rauh, A. Antov, R. A. Flavell, L. M. Sly, and G. Krystal SHIP Represses the Generation of IL-3-Induced M2 Macrophages by Inhibiting IL-4 Production from Basophils J. Immunol., September 15, 2009; 183(6): 3652 - 3660. [Abstract] [Full Text] [PDF] |
||||
![]() |
K. Ohmori, Y. Luo, Y. Jia, J. Nishida, Z. Wang, K. D. Bunting, D. Wang, and H. Huang IL-3 Induces Basophil Expansion In Vivo by Directing Granulocyte-Monocyte Progenitors to Differentiate into Basophil Lineage-Restricted Progenitors in the Bone Marrow and by Increasing the Number of Basophil/Mast Cell Progenitors in the Spleen J. Immunol., March 1, 2009; 182(5): 2835 - 2841. [Abstract] [Full Text] [PDF] |
||||
