The Journal of Experimental Medicine
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Published online 10 April 2006 doi:10.1084/jem.20051615
Rockefeller University Press, 0022-1007 $8.00
JEM, Volume 203, Number 4, 1105-1116
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ARTICLE

 Identification of an interleukin (IL)-25–dependent cell population that provides IL-4, IL-5, and IL-13 at the onset of helminth expulsion

Padraic G. Fallon1, Sarah J. Ballantyne2, Niamh E. Mangan1, Jillian L. Barlow2, Ayan Dasvarma2, Duncan R. Hewett2, Ann McIlgorm2, Helen E. Jolin2, and Andrew N.J. McKenzie2

1 Department of Biochemistry, Trinity College, Dublin 2, Ireland
2 Medical Research Council Laboratory of Molecular Biology, Cambridge CB2 2QH, England, UK

CORRESPONDENCE Andrew N. J. McKenzie: anm{at}mrc-lmb.cam.ac.uk

Type 2 immunity, which involves coordinated regulation of innate and adaptive immune responses, can protect against helminth parasite infection, but may lead to allergy and asthma after inappropriate activation. We demonstrate that il25–/– mice display inefficient Nippostrongylus brasiliensis expulsion and delayed cytokine production by T helper 2 cells. We further establish a key role for interleukin (IL)-25 in regulating a novel population of IL-4–, IL-5–, IL-13–producing non–B/non–T (NBNT), c-kit+, Fc{varepsilon}R1– cells during helminth infection. A deficit in this population in il25–/– mice correlates with inefficient N. brasiliensis expulsion. In contrast, administration of recombinant IL-25 in vivo induces the appearance of NBNT, c-kit+, Fc{varepsilon}R1– cells and leads to rapid worm expulsion that is T and B cell independent, but type 2 cytokine dependent. We demonstrate that these IL-25–regulated cells appear rapidly in the draining lymph nodes, implicating them as a source of type 2 cytokines during initiation of worm expulsion.

Abbreviations used: MLN, mesenteric lymph node; NBNT, non–B, non–T.

P.G. Fallon, S.J. Ballantyne, and N.E. Mangan contributed equally to this work.


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