T1/ST2-deficient Mice Demonstrate the Importance of T1/ST2 in Developing Primary T Helper Cell Type 2 Responses

doi:10.1084/jem.191.6.1069

Published online 20 March 2000.

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© The Rockefeller University Press, 0022-1007/2000/3/1069/ $5.00
The Journal of Experimental Medicine, Volume 191, Number 6, March 20, 2000 1069-1076

Brief Definitive Report

T1/ST2-deficient Mice Demonstrate the Importance of T1/ST2 in Developing Primary T Helper Cell Type 2 Responses

Michael J. Townsend^a, Padraic G. Fallon^b, David J. Matthews^a, Helen E. Jolin^a, and Andrew N.J. McKenzie^a
^a Medical Research Council Laboratory of Molecular Biology, Cambridge CB2 2QH, United Kingdom
^b Department of Pathology, University of Cambridge, Cambridge CB2 1QP, United Kingdom

Correspondence to: Andrew N.J. McKenzie, MRC Laboratory of Molecular Biology, Hills Rd., Cambridge, CB2 2QH, UK. Tel:44-1223-402350 Fax:44-1223-412178 E-mail:anm{at}mrc-lmb.cam.ac.uk.

Released online: 20 March 2000

We have generated mice with a deficiency in T1/ST2 expressionto clarify the roles of T1/ST2 in T helper cell type 2 (Th2)responses. Using immunological challenges normally characterizedby a Th2-like response, we have compared the responses of T1/ST2-deficientmice with those generated by wild-type mice. Using a primarypulmonary granuloma model, induced with Schistosoma mansonieggs, we demonstrate that granuloma formation, characterizedby eosinophil infiltration, is abrogated in T1/ST2-deficientmice. Furthermore, we clearly demonstrate that in the absenceof T1/ST2 expression, the levels of Th2 cytokine productionare severely impaired after immunization. Thus, in a secondarypulmonary granuloma model, draining lymph node cells from theT1/ST2-deficient animals produced significantly reduced levelsof IL-4 and IL-5, despite developing granulomas of a magnitudesimilar to those of wild-type mice and comparable antigen-specificimmunoglobulin isotype production. These data clearly demonstratethat T1/ST2 expression plays a role in the development of Th2-likecytokine responses and indicate that effector functions areinhibited in its absence.

Key Words: T1/ST2, T helper type 2 cells, immunoglobulin, pulmonary inflammation,mast cells

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