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 language | English (US) |
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Pages (from-to) | 1201-1209 |
Number of pages | 9 |
Journal | International Immunology |
Volume | 20 |
Issue number | 9 |
DOIs | |
State | Published - 2008 |
Externally published | Yes |
Keywords
- Apoptosis
- Basophils
- IL-3
- Parasitic helminth
ASJC Scopus subject areas
- Immunology and Allergy
- Immunology