The APPEESFRS Peptide, Restricted by the HLA-B*35:01 Molecule, and the APPEESFRF Variant Derived from an Autologous HIV-1 Strain Induces Polyfunctional Responses in CD8+ T Cells
Autor: | Liliana Acevedo-Sáenz, Paula Andrea Velilla-Hernández, L María Teresa Rugeles, Liseth Carmona-Pérez, Julio C. Delgado |
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Rok vydání: | 2015 |
Předmět: |
chemistry.chemical_classification
functional profile human immunodeficiency virus medicine.medical_treatment lcsh:R lcsh:Medicine Peptide Biology HIV-specific CD8+ T-cells General Biochemistry Genetics and Molecular Biology Epitope Cytokine lcsh:Biology (General) chemistry Immunology medicine peptides Cytotoxic T cell Tumor necrosis factor alpha Interferon gamma lcsh:QH301-705.5 Macrophage inflammatory protein CD8 Rapid Communication medicine.drug |
Zdroj: | BioResearch Open Access BioResearch Open Access, Vol 4, Iss 1, Pp 115-120 (2015) |
ISSN: | 2164-7844 |
Popis: | Numerous reports have focused on consensus peptides to determine CD8+ T-cell responses; however, few studies evaluated the functional profile using peptides derived from circulating strains of a specific region. We determined the effector profile and maturation phenotype of CD8+ T-cells targeting the consensus APPEESFRS (AS9) epitope and its variant APPEESFRF (AF9), previously identified. The free energy of binding, maturation phenotype, and polyfunctional profile of both peptides were similar. The magnitude of CD8+ T-cell responses to AF9 was greater than the one elicited by AS9, although the difference was not significant. The polyfunctional profile of AF9 was characterized by CD107a/interleukin-2 (IL-2)/macrophage inflammatory protein beta (MIP1β) and by interferon gamma (IFNγ)/MIP1β/tumor necrosis factor alpha (TNFα) in response to AS9. TNFα production was significantly higher in response to AF9 than to AS9, and there was a negative correlation between the absolute number of CD8+ T-cell-producing TNFα and the plasma human immunodeficiency virus (HIV) load, suggesting a role of this cytokine in the control of HIV replication. |
Databáze: | OpenAIRE |
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