Background: The CD5 protein antagonizes phosphorylation events downstream of T cell receptor (TCR) engagement\nto decrease T cell responsiveness. CD5-negative T cell clones respond preferentially over their CD5+ counterparts\nagainst cells with low human histocompatibility-linked leukocyte antigen (HLA) levels. In human immunodeficiency\nvirus type 1 (HIV-1) infection, CD5?CD8+ T cells increase in prevalence with disease progression.\nMethods: To investigate potential causes of this expansion of CD5?CD8+ T cells in HIV-1 infection, we compared CD5\nexpression on CD8+ T cells reactive against HIV-1 peptides, common viral peptides and a self peptide that together\nspan a broad range of TCR avidities in the context of the common HLA-A2 class I restriction molecule. Following\nstimulation, CD5 expression on peptide-specific CD8+ T cells was assessed by flow cytometry.\nResults: In healthy controls, there was no significant difference in the CD5+ percentage of CD8+ T cells specific for\ncommon viral peptides, but a lower percentage of those responding against a common self peptide expressed CD5.\nThe same relationship occurred in HIV-infected individuals, however, a lower percentage of HIV peptide-specific CD8+\nT cells than other viral peptide-specific CD8+ T cells expressed CD5. In terms of overall CD5 expression level at the\npeptide-specific responder population level, HIV-specific CD8+ T cells resembled those responsive against the self\npeptide, despite much higher avidity TCR/HLA/peptide interactions.\nConclusions: This deficit in CD5 expression selective for HIV-specific CD8+ T cells is consistent with in vivo adaptation\nto low avidity HIV peptide variants and has potential consequences for CD8+ T cell expansion, cross-reactivity and\nautoreactivity.
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