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Journal of Virology, April 2005, p. 4700-4708, Vol. 79, No. 8
0022-538X/05/$08.00+0     doi:10.1128/JVI.79.8.4700-4708.2005
Copyright © 2005, American Society for Microbiology. All Rights Reserved.

Virus-Specific and Bystander CD8 T Cells Recruited during Virus-Induced Encephalomyelitis

Audrey M. Chen,1 Nivedita Khanna,1,{dagger} Stephen A. Stohlman,1,2,3 and Cornelia C. Bergmann1,3*

Departments of Neurology,1 Molecular Microbiology and Immunology,2 Pathology, Keck School of Medicine, University of Southern California, Los Angeles, California3

Received 5 August 2004/ Accepted 22 November 2004

Neurotropic coronavirus-induced encephalitis was used to evaluate recruitment, functional activation, and retention of peripheral bystander memory CD8+ T cells. Mice were first infected with recombinant vaccinia virus expressing a non-cross-reactive human immunodeficiency virus (HIV) epitope, designated p18. Following establishment of an endogenous p18-specific memory CD8+ T-cell population, mice were challenged with coronavirus to directly compare recruitment, longevity, and activation characteristics of both primary coronavirus-specific and bystander memory populations trafficking into the central nervous system (CNS). HIV-specific memory CD8+ T cells were recruited early into the CNS as components of the innate immune response, preceding CD8+ T cells specific for the dominant coronavirus epitope, designated pN. Although pN-specific T-cell numbers gradually exceeded bystander p18-specific CD8+ T-cell numbers, both populations peaked concurrently within the CNS. Nevertheless, coronavirus-specific CD8+ T cells were preferentially retained. By contrast, bystander CD8+ T-cell numbers declined to background numbers following control of CNS virus replication. Furthermore, in contrast to highly activated pN-specific CD8+ T cells, bystander p18-specific CD8+ T cells recruited to the site of inflammation maintained a nonactivated memory phenotype and did not express ex vivo cytolytic activity. Therefore, analysis of host CD8+ T-cell responses to unrelated infections demonstrates that bystander memory CD8+ T cells can comprise a significant proportion of CNS inflammatory cells during virus-induced encephalitis. However, transient CNS retention and the absence of activation suggest that memory bystander CD8+ T cells may not overtly contribute to pathology in the absence of antigen recognition.

* Corresponding author. Mailing address: University of Southern California Keck School of Medicine, 1333 San Pablo St., MCH 148, Los Angeles, CA 90033. Phone: (323) 442-1062. Fax: (323) 225-2369. E-mail: cbergman{at}usc.edu.

{dagger} Present address: Division of Clinical Sciences, University of Toronto, Toronto, Canada M5S1A8.

Journal of Virology, April 2005, p. 4700-4708, Vol. 79, No. 8
0022-538X/05/$08.00+0     doi:10.1128/JVI.79.8.4700-4708.2005
Copyright © 2005, American Society for Microbiology. All Rights Reserved.



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