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Diminished secondary CTL response in draining lymph nodes on cutaneous challenge with herpes simplex virus

Department of Pathology and Immunology, Monash Medical School, Commercial Road, Prahran, Victoria 3181, Australia¹
Department of Microbiology and Immunology, Louisiana State University Medical Center, School of Medicine in Shreveport, Shreveport, LA 71130, USA²
Immunology Division, The Walter and Eliza Hall Institute of Medical Research, P.O. Royal Melbourne Hospital, Parkville, Victoria 3050, Australia³

Authors for correspondence: (i) Francis Carbone. Fax +61 3 9903 0731. e-mail carbone{at}med.monash.edu.au(ii) William Heath. Fax +61 3 9347 0852. e-mail heath@wehi.edu.au

We have shown that C57BL/6-derived CD8⁺ CTL specific for an immunodominant herpes simplex virus type 1 (HSV-1) glycoprotein B (gB) determinant express a highly conserved V10/junctional sequence combination. This extreme T cell receptor -chain bias can be used to track the activation of gB-specific CTL in lymph nodes draining the site of HSV-1 infection. In this report we have examined the accumulation of gB-specific CTL in the primary and secondary or recall CTL responses to HSV-1 infection. We found that gB-specific cytolytic activity present within popliteal lymph nodes draining HSV-infected foot-pads peaked at day 5 post-infection during the primary response. As found previously, this correlates with the accumulation of V10⁺CD8⁺ CTL in the activated T cell subset. Lymph node-derived cytotoxicity peaked between days 3 and 4 on secondary challenge with virus and, somewhat surprisingly, was considerably below that seen in the primary response. This reduced gB-specific cytolytic activity mirrored a near absence of V10⁺CD8⁺ T cell enrichment found within the draining lymph nodes during this recall response, consistent with the overall diminution of gB-specific CTL accumulation in this site. Finally, there was a second wave of biased accumulation of V10⁺CD8⁺ activated T cells within the popliteal lymph nodes well after the resolution of infection in both the primary and secondary responses. These results are discussed in terms of preferential activation of virus-specific memory T cells directly in infected tissues during a secondary CTL response at the expense of draining lymphoid organs.

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				S. Suvas, U. Kumaraguru, C. D. Pack, S. Lee, and B. T. Rouse CD4+CD25+ T Cells Regulate Virus-specific Primary and Memory CD8+ T Cell Responses J. Exp. Med., September 15, 2003; 198(6): 889 - 901. [Abstract] [Full Text] [PDF]