Diminished secondary CTL response in draining lymph nodes on cutaneous challenge with herpes simplex virus.
J Gen Virol
; 81(Pt 2): 407-14, 2000 Feb.
Article
en En
| MEDLINE
| ID: mdl-10644839
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 Vbeta10/junctional sequence combination. This extreme T cell receptor beta-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 Vbeta10(+)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 Vbeta10(+)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 Vbeta10(+)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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Colección:
01-internacional
Base de datos:
MEDLINE
Asunto principal:
Herpesvirus Humano 1
/
Linfocitos T CD8-positivos
/
Herpes Simple
Límite:
Animals
Idioma:
En
Revista:
J Gen Virol
Año:
2000
Tipo del documento:
Article
País de afiliación:
Australia
Pais de publicación:
Reino Unido