The Journal of Experimental Medicine
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Published 17 November 2003. doi:10.1084/jem.20031051
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© Rockefeller University Press, 0022-1007/2003/11/1583 $5.00
The Journal of Experimental Medicine, Volume 198, Number 10, 1583-1593

Memory CD8+ T Cells Provide Innate Immune Protection against Listeria monocytogenes in the Absence of Cognate Antigen

Rance E. Berg, Emily Crossley, Sean Murray and James Forman

Center for Immunology, University of Texas Southwestern Medical Center (UTSW), Dallas, TX 75390

Address correspondence to James Forman, University of Texas Southwestern Medical Center, Center for Immunology, 6000 Harry Hines Blvd., NA2.200, Dallas, TX 75390-9093. Phone: (214) 648-5924; Fax: (214) 648-5929; email: James.Forman{at}UTSouthwestern.edu

Interferon (IFN)-{gamma} plays an important role in the innate immune response against intracellular bacterial pathogens. It is commonly thought that natural killer cells are the primary source of this cytokine that is involved in activating antibacterial effects in infected cells and polarizing CD4+ T cells toward the Th1 subset. However, here we show that both effector and memory CD8+ T cells have the potential to secrete IFN-{gamma} in response to interleukin (IL)-12 and IL-18 in the absence of cognate antigen. We demonstrate that memory CD8+ T cells specific for the ovalbumin protein secrete IFN-{gamma} rapidly after infection with wild-type Listeria monocytogenes (LM). Furthermore, small numbers of ovalbumin-specific, memory CD8+ T cells can reduce spleen and liver bacterial counts in IFN-{gamma}–deficient mice 3 d after LM infection. Up-regulation of the receptors for IL-12 and IL-18 provides a mechanism for the ability of memory CD8+ T cells to respond in this antigen nonspecific manner. Thus, CD8+ T cells play an important role in the innate immune response against intracellular pathogens by rapidly secreting IFN-{gamma} in response to IL-12 and IL-18.

Key Words: innate immunity • T lymphocytes • cytokines • Listeria monocytogenes • IFN-{gamma}


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