{"entity": "publication", "iuid": "94824cd2469e493fad1c3bc5f25a614b", "timestamp": "2026-08-29T04:36:58.933Z", "links": {"self": {"href": "https://publications-affiliated.scilifelab.se/publication/94824cd2469e493fad1c3bc5f25a614b.json"}, "display": {"href": "https://publications-affiliated.scilifelab.se/publication/94824cd2469e493fad1c3bc5f25a614b"}}, "title": "The MHC-E peptide ligands for checkpoint CD94/NKG2A are governed by inflammatory signals, whereas LILRB1/2 receptors are peptide indifferent.", "authors": [{"family": "Middelburg", "given": "Jim", "initials": "J"}, {"family": "Ghaffari", "given": "Soroush", "initials": "S"}, {"family": "Schoufour", "given": "Tom A W", "initials": "TAW"}, {"family": "Sluijter", "given": "Marjolein", "initials": "M"}, {"family": "Schaap", "given": "Gaby", "initials": "G"}, {"family": "G\u00f6yn\u00fck", "given": "B\u00fcsra", "initials": "B"}, {"family": "Sala", "given": "Benedetta M", "initials": "BM"}, {"family": "Al-Tamimi", "given": "Lejla", "initials": "L"}, {"family": "Scheeren", "given": "Ferenc", "initials": "F"}, {"family": "Franken", "given": "Kees L M C", "initials": "KLMC"}, {"family": "Akkermans", "given": "Jimmy J L L", "initials": "JJLL"}, {"family": "Cabukusta", "given": "Birol", "initials": "B"}, {"family": "Joosten", "given": "Simone A", "initials": "SA"}, {"family": "Derksen", "given": "Ian", "initials": "I"}, {"family": "Neefjes", "given": "Jacques", "initials": "J"}, {"family": "van der Burg", "given": "Sjoerd H", "initials": "SH"}, {"family": "Achour", "given": "Adnane", "initials": "A"}, {"family": "Wijdeven", "given": "Ruud H M", "initials": "RHM"}, {"family": "Weidanz", "given": "Jon", "initials": "J"}, {"family": "van Hall", "given": "Thorbald", "initials": "T"}], "type": "journal article", "published": "2023-12-26", "journal": {"title": "Cell Reports", "issn": "2211-1247", "volume": "42", "issue": "12", "pages": "113516", "issn-l": null}, "abstract": "The immune checkpoint NKG2A/CD94 is a promising target for cancer immunotherapy, and its ligand major histocompatibility complex E (MHC-E) is frequently upregulated in cancer. NKG2A/CD94-mediated inhibition of lymphocytes depends on the presence of specific leader peptides in MHC-E, but when and where they are presented in situ is unknown. We apply a nanobody specific for the Qdm/Qa-1b complex, the NKG2A/CD94 ligand in mouse, and find that presentation of Qdm peptide depends on every member of the endoplasmic reticulum-resident peptide loading complex. With a turnover rate of 30 min, the Qdm peptide reflects antigen processing capacity in real time. Remarkably, Qdm/Qa-1b complexes require inflammatory signals for surface expression in situ, despite the broad presence of Qa-1b molecules in homeostasis. Furthermore, we identify LILRB1 as a functional inhibition receptor for MHC-E in steady state. These data provide a molecular understanding of NKG2A blockade in immunotherapy and assign MHC-E as a convergent ligand for multiple immune checkpoints.", "doi": "10.1016/j.celrep.2023.113516", "pmid": "38048225", "labels": [], "xrefs": [{"db": "pii", "key": "S2211-1247(23)01528-0"}], "notes": [], "created": "2026-08-20T07:52:02.836Z", "modified": "2026-08-20T07:52:02.850Z"}