Cutting edge: basophils are transiently recruited into the draining lymph nodes during helminth infection via IL-3, but infection-induced Th2 immunity can develop without basophil lymph node recruitment or IL-3.
Basophils are recognized as immune modulators through their ability to produce IL-4, a key cytokine required for Th2 immunity. It has also recently been reported that basophils are transiently recruited into the draining lymph node (LN) after allergen immunization and that the recruited basophils promote the differentiation of naive CD4 T cells into Th2 effector cells. Using IL-3(-/-) and IL-3Rbeta(-/-) mice, we report in this study that the IL-3/IL-3R system is absolutely required to recruit circulating basophils into the draining LN following helminth infection. Unexpectedly, the absence of IL-3 or of basophil LN recruitment played little role in helminth-induced Th2 immune responses. Moreover, basophil depletion in infected mice did not diminish the development of IL-4-producing CD4 T cells. Our results reveal a previously unknown role of IL-3 in recruiting basophils to the LN and demonstrate that basophils are not necessarily associated with the development of Th2 immunity during parasite infection.
Kim
Sohee
S
Department of Immunology, Lerner Research Institute, Cleveland Clinic Foundation, Cleveland, OH 44195, USA.
Prout
Melanie
M
Ramshaw
Hayley
H
Lopez
Angel F
AF
LeGros
Graham
G
Min
Booki
B
D000818:Animals; D001491:Basophils / Q000276:immunology* / Q000469:parasitology / Q000473:pathology*; D002465:Cell Movement / Q000235:genetics / Q000276:immunology*; D055879:Gene Knock-In Techniques; D007377:Interleukin-3 / Q000172:deficiency / Q000235:genetics / Q000502:physiology*; D008198:Lymph Nodes / Q000276:immunology* / Q000473:pathology*; D051379:Mice; D008807:Mice, Inbred BALB C; D018345:Mice, Knockout; D009559:Nippostrongylus / Q000276:immunology; D016185:Receptors, Interleukin-3 / Q000172:deficiency / Q000235:genetics / Q000502:physiology; D017206:Strongylida Infections / Q000276:immunology* / Q000469:parasitology / Q000473:pathology; D018418:Th2 Cells / Q000276:immunology* / Q000469:parasitology
D007377:Interleukin-3; D016185:Receptors, Interleukin-3