The Loss of HLA-F/KIR3DS1 Ligation Is Mediated by Hemoglobin Peptides.

ABSTRACT: The human leukocyte antigen (HLA)-Ib molecule, HLA-F, is known as a CD4+ T-cell protein and mediator of HIV progression. While HLA-Ia molecules do not have the chance to select and present viral peptides for immune recognition due to protein downregulation, HLA-F is upregulated. Post HIV infection, HLA-F loses the affinity to its activating receptor KIR3DS1 on NK cells leading to progression of the HIV infection. Several studies aimed to solve the question of the biophysical interface between HLA ligands and their cognate receptors. It became clear that even an invariant HLA molecule can be structurally modified by the variability of the bound peptide. We recently discovered the ability of HLA-F to select and present peptides and the HLA-F allele-specific peptide selection from the proteom

SUBMITTER: Ho GT 

PROVIDER: S-EPMC7672607 | biostudies-literature | 2020 Oct

REPOSITORIES: biostudies-literature