ArticleFrontiers in immunology2015
Polyclonal Expansion of NKG2C(+) NK Cells in TAP-Deficient Patients.
Article in Frontiers in immunology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 26 citations in OpenAlex.
- Inborn errors of immunity affecting the MHC class I pathway for antigen presentation.Journal of human immunity · 2025Review
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- Natural Killer Cell Engagers (NKCEs): a new frontier in cancer immunotherapy.Frontiers in immunology · 2023Review
- Anti-NKG2C/IL-15/anti-CD33 killer engager directs primary and iPSC-derived NKG2CMolecular therapy : the journal of the American Society of Gene Therapy · 2021Article
- HLA Class I Molecules as Immune Checkpoints for NK Cell Alloreactivity and Anti-Viral Immunity in Kidney Transplantation.Frontiers in immunology · 2021Review
- Atypical immune phenotype in severe combined immunodeficiency patients with novel mutations in IL2RG and JAK3.Genes and immunity · 2020Article
- NK Cells from RAG- or DCLRE1C-Deficient Patients Inhibit HCMV.Microorganisms · 2019Article
- Conserved and variable natural killer cell receptors: diverse approaches to viral infections.Immunology · 2019Review
- Review
- Alessandro Moretta and Transporter Associated With Antigen Processing (TAP) Deficiency: On Giant's Shoulders.Frontiers in immunology · 2019Article
- Stable Frequencies of HLA-CFrontiers in immunology · 2018Article
- Late Development of FcεRγFrontiers in immunology · 2018Article
- Deciphering the killer-cell immunoglobulin-like receptor system at super-resolution for natural killer and T-cell biology.Immunology · 2017Review
- Harnessing adaptive natural killer cells in cancer immunotherapy.Molecular oncology · 2015Review
Corrections and comments
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Authors and funding
9 authors at 5 institutions in 4 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Adaptive natural killer (NK) cell responses to human cytomegalovirus infection are characterized by the expansion of NKG2C(+) NK cells expressing self-specific inhibitory killer-cell immunoglobulin-like receptors (KIRs). Here, we set out to study the HLA class I dependency of such NKG2C(+) NK cell expansions. We demonstrate the expansion of NKG2C(+) NK cells in patients with transporter associated with antigen presentation (TAP) deficiency, who express less than 10% of normal HLA class I levels. In contrast to normal individuals, expanded NKG2C(+) NK cell populations in TAP-deficient patients display a polyclonal KIR profile and remain hyporesponsive to HLA class I-negative target cells. Nonetheless, agonistic stimulation of NKG2C on NK cells from TAP-deficient patients yielded significant responses in terms of degranulation and cytokine production. Thus, while interactions with self-HLA class I molecules likely shape the KIR repertoire of expanding NKG2C(+) NK cells during adaptive NK cell responses in normal individuals, they are not a prerequisite for NKG2C(+) NK cell expansions to occur. The emergence of NKG2C-responsive adaptive NK cells in TAP-deficient patients may contribute to antiviral immunity and potentially explain these patients' low incidence of severe viral infections.
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