Ask about this productRelated genes to: KLRC1 Blocking Peptide
- Gene:
- KLRC1 NIH gene
- Name:
- killer cell lectin like receptor C1
- Previous symbol:
- NKG2
- Synonyms:
- NKG2-A, NKG2-B, CD159a
- Chromosome:
- 12p13
- Locus Type:
- gene with protein product
- Date approved:
- 1998-01-16
- Date modifiied:
- 2016-01-14
Related products to: KLRC1 Blocking Peptide
Related articles to: KLRC1 Blocking Peptide
- Mitochondrial function is essential for biology, particularly in cancer. However, cell-type-specific expression patterns of conserved mitochondrial genes in gastric cancer (GC) remain unclear. We herein raised and tested a novel hypothesis of "mitochondrial conserved gene expression homeostasis imbalance" in GC cohorts with single-cell resolution. - Source: PubMed
Publication date: 2026/06/17
Chang LeHou JingwenLi YingyingLiu SimengFeng PengyaLi YaQiu ChunjingZheng PengyuanXue XiaMi Yang - Pancreatic ductal adenocarcinoma (PDAC) has a profoundly immunosuppressive tumour microenvironment (TME) that limits anti-tumour immunity and contributes to resistance to immunotherapy. Although γδ T-cells can integrate innate and adaptive immune signals, their abundance, transcriptional states and regulatory pathways in PDAC remain incompletely defined. We performed integrated single-cell RNA sequencing analysis of 39 pancreatic tissue samples, comprising 33 PDAC tumours and 6 adjacent normal tissues. After dataset integration, immune cell annotation, and stringent per-cell gating, γδ T-cells were quantified and profiled for checkpoint-, ligand-, and chemokine-related programmes. γδ T-cells were detectable across PDAC samples but showed substantial inter-sample heterogeneity in abundance. Among candidate inhibitory pathways, , , and expression in γδ T-cells did not differ significantly between tumour and adjacent tissues, whereas (encoding NKG2A) showed a tumour-associated difference at the single-cell level, with a consistent directional pattern in sample-level summaries. NKG2A expression was comparable between γδ T-cells and NK cells, suggesting a shared inhibitory programme. HLA-E, the ligand for NKG2A, showed higher epithelial-cell expression in tumour than adjacent tissue in sample-level summaries (median 1.06 vs. 0.57; BH-q = 0.035). Chemokine analysis identified enrichment of CCL2, CCL4, CCL5, CXCL8 and CXCL12, with limited CXCL9/10/11 signalling within the PDAC TME. Within γδ T-cells, CXCR4 was the trafficking receptor, followed by CCR6, CCR7 and CXCR6. PDAC-infiltrating γδ T-cells show marked inter-sample heterogeneity and variable inhibitory and trafficking-related programmes. Integrated transcriptomic analysis nominates HLA-E-NKG2A as a candidate regulatory axis, with NK cells included as a biologically relevant comparator. Chemokine receptor patterns, particularly CXCR4, CCR6, CCR7 and CXCR6, suggest candidate trafficking features. These findings are hypothesis-generating and require spatial, protein-level and functional validation. - Source: PubMed
Publication date: 2026/05/25
Mandal SaikatHasan Shirin RDhali ArkadeepMaji Manideepa - Multiple myeloma (MM) develops through asymptomatic precursor stages characterized by progressive remodeling of the bone marrow (BM) immune microenvironment and disruption of bone homeostasis. To delineate changes in natural killer (NK) cell states during disease evolution, we investigated coordinated immune-tumor remodeling by integrating NK cell functional states with plasma cell-intrinsic susceptibility programs derived from CRISPR-based screens across healthy donors (HD), monoclonal gammopathy of undetermined significance (MGUS), smoldering MM (SMM), and newly diagnosed MM patients. The integration of NK cell state-associated gene signatures with plasma cell transcriptional programs revealed stage-specific co-variation between immune and tumor compartments. Public single-cell RNA sequencing datasets were interrogated to resolve NK cell heterogeneity, identifying cytotoxic CD56 and regulatory CD56 subsets. NK cell dynamics displayed stage-dependent changes, with early expansion followed by the contraction of CD56 cells in BM, whereas CD56 cells showed predominantly compositional remodeling. Within the CD56 subset, transcriptional changes included an increased expression of (encoding NKG2A), subsequently validated by multiparametric flow cytometry. In parallel, plasma cell programs associated with NK sensitivity progressively decreased along disease stages, supporting tumor adaptation to immune pressure. The NKG2A ligand HLA-E displayed selective expression within CD16 monocytes and followed a distinct variable pattern across disease stages, highlighting a microenvironmental contribution to NK cell regulation. Collectively, these findings indicate a coordinated process of immune-tumor co-evolution, characterized by dynamic remodeling of NK cell states and plasma cell susceptibility, with the NKG2A-HLA-E axis emerging as a central interface during MM progression. - Source: PubMed
Publication date: 2026/05/22
Aquilina CristinaRomano AndreaCorsale Anna MariaBiondo MartaSpeciale MariaTofacchi ElenaDi Simone MartaGigliotta EmiliaDieli CostanzaAvellone ClaudiaToscano AngeloCamarda LawrenceRomano AlessandraCambria DanielaGiavaresi GianlucaRaimondi LaviniaNeri AntoninoCampana StefaniaCaccamo NadiaDieli FrancescoSiragusa SergioMeraviglia SerenaBotta Cirino - Natural killer (NK) cell-targeting immunotherapies are emerging, yet the differentiation and functional states of tumor-infiltrating NK cells remain poorly understood. Using matched single-nucleus RNA and ATAC sequencing of samples from patients with non-small cell lung cancer (NSCLC), we resolved the transcriptional and epigenetic landscape of intratumoral NK cells. We identified two tumor-associated NK (taNK) cell subsets marked by expression of (CD103) and (CD49a) that display features of tissue residency and dysfunction while preserving cytotoxic function. Trajectory and regulon analyses revealed an inflammation-driven transition from early () NK cells toward an (CD39) effector state characterized by interferon-stimulated gene (ISG) programs. Functional profiling established CD39 taNK cells as the dominant cytotoxic NK cell population with superior killing capacity that was further potentiated by NKG2A blockade. This study offers mechanistic insights into NK cell differentiation in NSCLC and establishes CD39 taNK cells as a targetable effector population for immunotherapy. - Source: PubMed
Publication date: 2026/06/05
Serger ClaraRebuffet LucasSandholzer Michael TRackwitz WiebkeFusi IreneHerzig PetraBrüggemann AnnaleaPawlow Carina AChichelnitskiy EvgenyHajnal DanielOelgarth NicoleUzun SarpSchultheiß ChristophZingg AndreasTundo SofiaLuu Thuy THojski AljazLardinois DidierNeubert LaviniaBinder MaschaMertz KirstenTrefny Marcel PKirchhammer NicoleNatoli MarinaMatter Matthias SLäubli HeinzFalk ChristineSchaeuble KarinVivier EricRomagnani AndreaZippelius Alfred - The success of NK cell therapies against solid tumors remains limited, possibly due to tumor resistance mechanisms associated with the upregulation of inhibitory ligands. Previous studies have demonstrated that expanded NK cells can lyse ovarian cancer cells and produce IFN-γ. However, secretion of IFN-γ within the tumor microenvironment, leads to the upregulation of both classical HLA class I and the non-classical HLA-E on bystander tumor cells, thereby contributing to resistance against NK cell-mediated cytotoxicity. To overcome this IFN-γ induced resistance, we developed NKG2A-knockout NK: TCR cells targeting PRAME (NK: PRAME), a tumor-associated antigen expressed in ovarian cancer. - Source: PubMed
Publication date: 2026/06/04
van Hees Els PRensing Oliva WHagedoorn Renate SPothast Cilia RWouters Anne Kvan Amerongen Rosa AFalkenburg J H Frederikde Groot RosaHeemskerk Mirjam H M