The Journal of Experimental Medicine
VeriKine-HS Human IFN-Beta
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© The Rockefeller University Press, 0022-1007/1998/3/787/ $5.00
The Journal of Experimental Medicine, Volume 187, Number 5, March 2, 1998 787-794

Articles

Selective Expression of a Stable Cell Surface Molecule on Type 2 but Not Type 1 Helper T Cells

Damo Xu*, Woon Ling Chan{ddagger}, Bernard P. Leung*, Fang-ping Huang*, Rachel Wheeler{ddagger}, David Piedrafita*, John H. Robinson§, and Foo Y. Liew*

From the * Department of Immunology, University of Glasgow, Glasgow G11 6NT, United Kingdom; the {ddagger} Department of Virology, St. Bartholomew and Royal London School of Medicine, QMW College, University of London, London EC1A 7BE, United Kingdom; and the § Department of Immunology, University of Newcastle, Newcastle Upon Tyne NE2 4HH, United Kingdom

T helper cell type 1 (Th1) and 2 (Th2) are central to immune regulation. However, no stable cell surface marker capable of distinguishing and separating these two subsets of CD4+ cells has yet been found. Using differential display PCR, we have identified a gene encoding a cell membrane bound molecule, originally designated ST2L, T1, DER4, or Fit, expressed constitutively and stably on the surface of murine Th2s, but not Th1s even after stimulation with a range of immunological stimuli. Antibody against a peptide derived from ST2L strongly and stably labeled the surface of cloned Th2s but not Th1s, and Th2s but not Th1s derived from naive T cells of ovalbumin T cell receptor–{alpha}/β transgenic mice. Three-color single cell flow cytometric analysis shows that cell surface ST2L coexpressed with intracellular interleukin (IL)-4, but not with interferon (IFN)-{gamma}. The antibody selectively lysed Th2s in vitro in a complement-dependent manner. In vivo, it enhanced Th1 responses by increasing IFN-{gamma} production and decreasing IL-4 and IL-5 synthesis. It induced resistance to Leishmania major infection in BALB/c mice and exacerbated collagen-induced arthritis in DBA/1 mice. Thus, ST2L is a stable marker distinguishing Th2s from Th1s and is also associated with Th2 functions. Hence, it may be a target for therapeutic intervention.

This work was supported by the Wellcome Trust, the Medical Research Council of the United Kingdom, The Joint Research Board of The Barts National Health Service Trust.

We thank Dr. Wanda Niedbala for some of the tissue culture, Dr. Alisdair Gracie for purifying the anti-ST2L antibody, Dr. Jim Cohen for use of fluorescent microscope, Dr. Nick Golding for advice on FACS® graphic, and Dr. Ken Murphy for the D011.10 transgenic mice.

Address correspondence to F.Y. Liew, Department of Immunology, University of Glasgow, Glasgow G11 6NT, UK. Phone: 44-141-211-2695; Fax: 44-141-337-3217; E-mail: f.y.liew{at}clinmed.gla.ac.uk

1 Abbreviations used in this paper: CIA, collagen-induced arthritis; DD-PCR, differential display PCR; mRNA, messenger RNA.


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