The Journal of Experimental Medicine
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Published online 27 January 2003 doi:10.1084/jem.20021683
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© Rockefeller University Press, 0022-1007/2003/2/387 $5.00
The Journal of Experimental Medicine, Volume 197, Number 3, 387-393

Brief Definitive Report

Immunotherapy of Cytotoxic T Cell–resistant Tumors by T Helper 2 Cells : An Eotaxin and STAT6-dependent Process



Joerg Mattes1, Mark Hulett2, Wei Xie2, Simon Hogan1, Marc E. Rothenberg3, Paul Foster1 and Christopher Parish2

1 Division of Molecular Bioscience, John Curtin School of Medical Research, Australian National University, Canberra ACT 2601, Australia
2 Division of Immunology and Genetics, John Curtin School of Medical Research, Australian National University, Canberra ACT 2601, Australia
3 Division of Allergy and Immunology, Department of Pediatrics, Children's Hospital Medical Center, Cincinnati, OH 45229

Address correspondence to Christopher Parish or Paul Foster, Division of Immunology and Genetics, John Curtin School of Medical Research, Australian National University, Canberra ACT 2601, Australia. Phone: 61-2-61252604; Fax: 61-2-61252595; E-mail: christopher.parish{at}anu.edu.au or paul.foster{at}anu.edu.au

Currently most attempts at cancer immunotherapy involve the generation of CD8+ cytotoxic T lymphocytes (CTLs) against tumor-associated antigens. Many tumors, however, have been immunoselected to evade recognition by CTLs and thus alternative approaches to cancer immunotherapy are urgently needed. Here we demonstrate that CD4+ T cells that recognize a secreted tumor-specific antigen and exhibit a cytokine secretion profile characteristic of Th2 cells, are capable of clearing established lung and visceral metastases of a CTL-resistant melanoma. Clearance of lung metastases by the Th2 cells was found to be totally dependent on the eosinophil chemokine, eotaxin, and partially dependent on the transcription activator signal transducer and activator of transcription 6 (STAT6), with degranulating eosinophils within the tumors inducing tumor regression. In contrast, tumor-specific CD4+ Th1 cells, that recruited macrophages into the tumors, had no effect on tumor growth. This work provides the basis for a new approach to adoptive T cell immunotherapy of cancer.

Key Words: Th2 cells • tumor immunotherapy • immune evasion • eosinophils • eotaxin


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