Abstract
Programmed death (PD)-1 and its ligand, PD-L1, are co-stimulatory molecules expressed on T cells and antigen-presenting cells, respectively, that modulate T cell receptor signals. Altered PD expression or signalling contributes to pathogen persistence in chronic infections. The sequence of the feline PD genes was derived from gene amplification with primers conserved across human and canine homologs, and by sequence extension through rapid amplification of cDNA ends. Feline PD-1 was similar to that of other mammalian species and consisted of extracellular, transmembrane and cytoplasmic regions. Functional motif analysis of the translated amino acid sequence predicted immunoreceptor tyrosine-based inhibitory and switch motifs, and a SH3-binding region, in the cytoplasmic tail. PD-1 and PD-L1 were expressed in resting lymphocytes and dendritic cells, and up-regulated on mitogen-activated or irradiated lymphocytes of both CD4 and CD8-positive subsets. In vitro infection with the feline immunodeficiency virus (FIV) significantly decreased PD-1, but not PD-L1, gene expression in lymphocytes at 24h, and decreased expression of both genes at 168h. No significant changes in gene or protein expression from FIV infection were noted in de...Continue Reading
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