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Infection and Immunity, April 2003, p. 1961-1971, Vol. 71, No. 4
0019-9567/03/$08.00+0     DOI: 10.1128/IAI.71.4.1961-1971.2003
Copyright © 2003, American Society for Microbiology. All Rights Reserved.

Signaling through the T1/ST2 Molecule Is Not Necessary for Th2 Differentiation but Is Important for the Regulation of Type 1 Responses in Nonhealing Leishmania major Infection

P. Kropf,1 S. Herath,1 R. Klemenz,2 and I. Müller1*

Division of Investigative Science, Department of Immunology, Faculty of Medicine, Imperial College of Science, Technology and Medicine, London, United Kingdom,1 Division of Cancer Research, Department of Pathology, University of Zürich, Zürich, Switzerland2

Received 29 July 2002/ Returned for modification 17 September 2002/ Accepted 2 January 2003

T1/ST2 is a stable cell surface marker selectively expressed on type 2 T helper (Th2) effector cells. Since nonhealing Leishmania major infections in susceptible BALB/c mice have been ascribed to a polarized Th2 response, we used an anti-T1/ST2 monoclonal antibody (MAb) or a T1-Fc fusion protein to investigate the role of CD4+ T1/ST2+ Th2 cells in experimental leishmaniasis. We show that interfering with T1/ST2 signaling had no effect on lesion development or parasite replication; however, it induced a significantly higher type 1 response and an enhanced capacity of CD4+ T cells to respond to interleukin 12 (IL-12). Surprisingly, even in the presence of an elevated Th1 response, the production of antigen-specific type 2 cytokines was not altered in the group of mice treated with the anti-T1/ST2 MAb or the T1-Fc fusion protein. To characterize further this Th2 response, we assessed the cytokine profile of CD4+ T cells and found that interfering with T1/ST2 signaling did not alter the cytokine profile of CD4+ T1/ST2+ T cells. These results show that T1/ST2 signaling is not necessary for the differentiation of naive CD4+ T cells into antigen-specific CD4+ T1/ST2+ Th2 cells. In addition to CD4+ T1/ST2+ T cells, we detected another subpopulation of CD4+ Th2 cells, negative for the expression of T1/ST2, that could differentiate in vivo in response to L. major infection. Taken together, our results suggest that CD4+ T1/ST2+ Th2 cells but not CD4+ T1/ST2- Th2 cells can downregulate the Th1 response during the course of a nonhealing L. major infection through a mechanism that is independent of IL-4 or IL-10.

* Corresponding author. Mailing address: Imperial College of Science, Technology and Medicine, Faculty of Medicine, Division of Investigative Science, Department of Immunology, Norfolk Place, London W21PG, United Kingdom. Phone: 44-20-7594 3732. Fax: 44-20-74020653. E-mail: i.muller{at}ic.ac.uk.

Editor: S. H. E. Kaufmann

Infection and Immunity, April 2003, p. 1961-1971, Vol. 71, No. 4
0019-9567/03/$08.00+0     DOI: 10.1128/IAI.71.4.1961-1971.2003
Copyright © 2003, American Society for Microbiology. All Rights Reserved.



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