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

Claerwen M. Jones, Stephen C. Cose, James M. McNally, Stephen R. Jennings, William R. Heath, Francis R. Carbone

Research output: Contribution to journalArticleResearchpeer-review

Abstract

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 VB1O/junctional sequence combination. This extreme T cell receptor B-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 VB1O+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 VB1O+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 VB1O+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.

Original languageEnglish
Pages (from-to)407-414
Number of pages8
JournalJournal of General Virology
Volume81
Issue number2
DOIs
Publication statusPublished - 1 Jan 2000

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