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The influence of macrophage inflammatory protein-1alpha on protective immunity mediated by antiviral cytotoxic T cells

Jones, Emma, Price, David, Dahm-Vicker, Michaela, Cerundolo, Vincenzo, Klenerman, Paul and Gallimore, Awen 2003. The influence of macrophage inflammatory protein-1alpha on protective immunity mediated by antiviral cytotoxic T cells. Immunology 109 (1) , pp. 68-75. 10.1046/j.1365-2567.2003.01636.x

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Abstract

Macrophage inflammatory protein 1α (MIP-1α), a member of the CC-chemokine subfamily, is known to induce chemotaxis of a variety of cell types in vivo. Although the role of MIP-1α in inflammatory responses generated following primary infection of mice with many different pathogens has been characterized, the influence of this chemokine on the generation of antigen-specific T-cell responses in vivo is less well understood. This is important, as virus-specific CD8+ T lymphocytes (CTL) play a crucial role in defence against viral infections, both acutely and in the long term. In this study, we compared the ability of wild-type and MIP-1α-deficient (MIP-1α−/−) mice to mount CTL responses specific for the immunodominant epitope derived from influenza nucleoprotein (NP366–374). Influenza-specific CTL responses were compared with respect to frequency, cytotoxic activity and ability to clear subsequent infections with recombinant vaccinia viruses expressing the influenza NP. The results indicate that antiviral CTL generated in MIP-1α−/− mice are slightly impaired in their ability to protect against a subsequent infection. However, impaired in vivo CTL-mediated antiviral protection was found to be associated with reduced cytotoxicity rather than with a failure of the CTL to migrate to peripheral sites of infection.

Item Type: Article
Date Type: Publication
Status: Published
Schools: Medicine
Subjects: Q Science > QR Microbiology > QR180 Immunology
Publisher: Wiley Blackwell
ISSN: 0019-2805
Date of First Compliant Deposit: 17 May 2016
Date of Acceptance: 17 February 2003
Last Modified: 04 Jun 2017 09:08
URI: http://orca.cf.ac.uk/id/eprint/90953

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