The Journal of Experimental Medicine
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© The Rockefeller University Press, 0022-1007/1998/12/2357/ $5.00
The Journal of Experimental Medicine, Volume 188, Number 12, December 21, 1998 2357-2368

Articles

The Central Role of CD4+ T Cells in the Antitumor Immune Response

Kenneth Hung*, Robert Hayashi§, Anne Lafond-Walker{ddagger}, Charles Lowenstein{ddagger}, Drew Pardoll*, and Hyam Levitsky*

From the * Department of Oncology and the {ddagger} Department of Cardiology, Johns Hopkins University School of Medicine, Baltimore, Maryland 21205; and the § Department of Pediatrics, Washington University School of Medicine, St. Louis, Missouri 63110

The induction of optimal systemic antitumor immunity involves the priming of both CD4+ and CD8+ T cells specific for tumor-associated antigens. The role of CD4+ T helper cells (Th) in this response has been largely attributed to providing regulatory signals required for the priming of major histocompatibility complex class I restricted CD8+ cytolytic T lymphocytes, which are thought to serve as the dominant effector cell mediating tumor killing. However, analysis of the effector phase of tumor rejection induced by vaccination with irradiated tumor cells transduced to secrete granulocyte/macrophage colony-stimulating factor indicates a far broader role for CD4+ T cells in orchestrating the host response to tumor. This form of immunization leads to the simultaneous induction of Th1 and Th2 responses, both of which are required for maximal systemic antitumor immunity. Cytokines produced by these CD4+ T cells activate eosinophils as well as macrophages that produce both superoxide and nitric oxide. Both of these cell types then collaborate within the site of tumor challenge to cause its destruction.

Key Words: cancer • vaccine • T helper cell • macrophage • eosinophil

Address correspondence to Hyam Levitsky, Johns Hopkins University School of Medicine, 347 Ross Bldg., 720 Rutland Ave., Baltimore, MD 21205. Phone: 410-614-0552; Fax: 410-614-9705; E-mail: hy{at}welchlink.welch.jhu.edu

1 Abbreviations used in this paper: iNOS, inducible nitric oxide synthase; NO, nitric oxide.


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