Comparison of Influenza and SIV Specific CD8 T Cell Responses in Macaques
AuthorJegaskanda, S; Reece, JC; De Rose, R; Stambas, J; Sullivan, L; Brooks, AG; Kent, SJ; Sexton, A
Source TitlePLoS One
PublisherPUBLIC LIBRARY SCIENCE
University of Melbourne Author/sJEGASKANDA, SINTHUJAN; REECE, JEANETTE; De Rose, Robert; Stambas, John; Sullivan, Lucy; Brooks, Andrew; Kent, Stephen; SEXTON, AMY; Reece, Jeanette
AffiliationMicrobiology and Immunology
Chemical and Biomolecular Engineering
Melbourne School of Population and Global Health
Document TypeJournal Article
CitationsJegaskanda, S., Reece, J. C., De Rose, R., Stambas, J., Sullivan, L., Brooks, A. G., Kent, S. J. & Sexton, A. (2012). Comparison of Influenza and SIV Specific CD8 T Cell Responses in Macaques. PLOS ONE, 7 (3), https://doi.org/10.1371/journal.pone.0032431.
Access StatusOpen Access
Macaques are a potentially useful non-human primate model to compare memory T-cell immunity to acute virus pathogens such as influenza virus and effector T-cell responses to chronic viral pathogens such as SIV. However, immunological reagents to study influenza CD8(+) T-cell responses in the macaque model are limited. We recently developed an influenza-SIV vaccination model of pigtail macaques (Macaca nemestrina) and used this to study both influenza-specific and SIV-specific CD8(+) T-cells in 39 pigtail macaques expressing the common Mane-A*10(+) (Mane-A01*084) MHC-I allele. To perform comparative studies between influenza and SIV responses a common influenza nucleoprotein-specific CD8(+) T-cell response was mapped to a minimal epitope (termed RA9), MHC-restricted to Mane-A*10 and an MHC tetramer developed to study this response. Influenza-specific memory CD8(+) T-cell response maintained a highly functional profile in terms of multitude of effector molecule expression (CD107a, IFN-γ, TNF-α, MIP-1β and IL-2) and showed high avidity even in the setting of SIV infection. In contrast, within weeks following active SIV infection, SIV-specific CD8(+) effector T-cells expressed fewer cytokines/degranulation markers and had a lower avidity compared to influenza specific CD8(+) T-cells. Further, the influenza specific memory CD8 T-cell response retained stable expression of the exhaustion marker programmed death-marker-1 (PD-1) and co-stimulatory molecule CD28 following infection with SIV. This contrasted with the effector SIV-specific CD8(+) T-cells following SIV infection which expressed significantly higher amounts of PD-1 and lower amounts of CD28. Our results suggest that strategies to maintain a more functional CD8(+) T-cell response, profile may assist in controlling HIV disease.
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