The Journal of Experimental Medicine
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© The Rockefeller University Press, 0022-1007/1999/10/895/ $5.00
The Journal of Experimental Medicine, Volume 190, Number 7, October 4, 1999 895-902

Original Article

Crucial Role of the Interleukin 1 Receptor Family Member T1/St2 in T Helper Cell Type 2–Mediated Lung Mucosal Immune Responses

Anthony J. Coylea, Clare Lloyda, Jane Tiana, Trang Nguyena, Christina Erikksonb, Lin Wanga, Par Ottosonb, Per Perssonb, Tracy Delaneya, Sophie Lehara, Steve Lina, Louis Poissona, Christian Meiselc,d, Thomas Kamradtc,d, Torbjorn Bjerkeb, Douglas Levinsona, and Jose Carlos Gutierrez-Ramosa

a Department of Biology, Inflammation Division, Millennium Pharmaceuticals, Inc., Cambridge, Massachusetts 02139
b Astra Draco, Inflammation Pharmacology, Preclinical Research and Development, S-221 00 Lund, Sweden
c Deutsches Rheumaforschungs Zentrum, Berlin D-10117, Germany
d Universitätsklinikum Charite, Rheumatologie und Klinische Immunologie, D-10098 Berlin, Germany
Inflammation Division, Millennium Pharmaceuticals, Inc., 75 Sidney St., Cambridge, MA 02139.617-551-8910617-679-7347

coyle{at}mpi.com

T1/ST2 is an orphan receptor of unknown function that is expressed on the surface of murine T helper cell type 2 (Th2), but not Th1 effector cells. In vitro blockade of T1/ST2 signaling with an immunoglobulin (Ig) fusion protein suppresses both differentiation to and activation of Th2, but not Th1 effector populations. In a nascent Th2-dominated response, anti-T1/ST2 monoclonal antibody (mAb) inhibited eosinophil infiltration, interleukin 5 secretion, and IgE production. To determine if these effects were mediated by a direct effect on Th2 cells, we next used a murine adoptive transfer model of Th1- and Th2-mediated lung mucosal immune responses. Administration of either T1/ST2 mAb or T1/ST2-Ig abrogated Th2 cytokine production in vivo and the induction of an eosinophilic inflammatory response, but failed to modify Th1-mediated inflammation. Taken together, our data demonstrate an important role of T1/ST2 in Th2-mediated inflammatory responses and suggest that T1/ST2 may prove to be a novel target for the selective suppression of Th2 immune responses.

Key Words: inflammation • eosinophil • asthma • cytokines • immunoglobulin superfamily

1used in this paper: BAL, bronchoalveolar lavage; CCR, CC chemokine receptor; TLR, Toll-like receptor

© 1999 The Rockefeller University Press


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