You are currently viewing the summary.
View Full TextLog in to view the full text
AAAS login provides access to Science for AAAS members, and access to other journals in the Science family to users who have purchased individual subscriptions.
More options
Download and print this article for your personal scholarly, research, and educational use.
Buy a single issue of Science for just $15 USD.
Summary
The human leukocyte antigen–E (HLAE) molecule is expressed on all nucleated cells and presents self-peptides. The resulting complexes can bind to inhibitory receptors on immune killer cells, including ∼50% of natural killer (NK) cells and a subset (∼5%) of CD8+ cytotoxic T lymphocytes (CTLs). Interruption of this inhibitory axis, which serves as an immune checkpoint, can improve effector functions of both CTLs and NK cells and enhance antitumor activity (1). HLA-E antigen expression can also be used as a mechanism for pathogen-infected cells to avoid being killed by NK cells. However, HLA-E can present peptides from pathogens and tumor cells to so-called unconventional CD8+ T cells, which can then be mobilized to fight the infection or tumor. Recent advances in understanding this dichotomy between unconventional T cell activation and NK cell suppression reveal potential preventive and therapeutic applications in infectious diseases and cancer.
This is an article distributed under the terms of the Science Journals Default License.