T cell-derived IL-3 plays key role in parasite infection-induced basophil production but is dispensable for in vivo basophil survival.
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.
Shen
Tao
T
Department of Immunology/NB30, Lerner Research Institute, Cleveland Clinic Foundation, 9500 Euclid Avenue, Cleveland, OH 44195, USA.
Kim
Sohee
S
Do
Jeong-su
JS
Wang
Lu
L
Lantz
Chris
C
Urban
Joseph F
JF
Le Gros
Graham
G
Min
Booki
B
D000818:Animals; D017209:Apoptosis; D001491:Basophils / Q000276:immunology* / Q000502:physiology; D007377:Interleukin-3 / Q000276:immunology / Q000378:metabolism*; D008213:Lymphocyte Activation / Q000276:immunology*; D051379:Mice; D008807:Mice, Inbred BALB C; D008810:Mice, Inbred C57BL; D009559:Nippostrongylus / Q000472:pathogenicity*; D017206:Strongylida Infections / Q000276:immunology* / Q000469:parasitology; D013601:T-Lymphocytes / Q000276:immunology* / Q000378:metabolism
D007377:Interleukin-3